Animal Physiology Midterm Ii

Front 1

Striated muscle

Back 1

sacromere, big cells with multiple nuclei
-skeletal muscle (controls body movement) and cardiac muscle (controls contraction of the heart)

Front 2

Smooth Muscle

Back 2

lines digestive tract and blood vessels
-1 nuceli per cell

Front 3

Connective tissue

Back 3

tendon: anchors muscle to bone
ligament: connects bone to bone
-part of skeletal muscle tissue structure

Front 4

Muscle Fiber

Back 4

long, cylindrical multinucleate cells, arranged in parallel
-> development: myoblast- myotube-> mature fiber

Front 5

Myofibrils

Back 5

parallel subunits of a muscle fiber (inside a cell)

Front 6

Sarcomeres

Back 6

subunit of myofibrils; functional unit of striated muscle which makes muscles appear striped
2 major filament types:
1. Thick filaments = myosin
- motor molecules that hydrolyze ATP
2. thin filaments = actin, troponin, and tropomyosin
actin-> globular beads (actin-G) polymerize to form double helix fibers (actin F)

Front 7

Motor Molecules

Back 7

allow chemomechanical transduction
1. Dyein: cylia, flagella, retrograde axonal transport (moving back from axon terminal to cell body)
2. Kinesin: anterograde axonal transport, cyotkinesis
3. Myosin: muscle contraction, cell movement, organelle transport

Front 8

Components of Sarcomere

Back 8

Z disk: border of sarcomere, composed of alpha-actin: site where actin is anchored
A band: dark region of thick filaments (where myosin is)
H zone: inner portion of A band containing only myosin
I band: light region between A bands containing only thin filaments (consists of 2 sarcomeres)

-Each actin is surrounded by 3 mysoin

Cross-bridges: extensions of myosin that bind with actin during muscle contraction

Front 9

Myofilament structure

Back 9

1. Thin Filament: beaded double helix of G-actin (globular)
- Tropomyosin: filament located in groove of actin double helix (1 tropomyosin/ 7 actin)
-Troponin complex: Ca2+ binding protein attached at intervals along tropomyosin- point where Ca2+ acts on thin filament
2. Thick filament:
-2 myosin heavy chains: long helical chain with globular head
-4 myosin light chains: -2 essential light chains: globular; -2 regulatory light chains: globular; binds myosin light chain kinases (MLCK)- important regulator!

-globular head = where cross-bridge forms -> thus each myosin can form 2 cross-bridges

Front 10

Sliding-filament theory

Back 10

Huxley and Neudergerke (1954)
-Light microscopy observations of muscle contraction
-contraction -> increase actin/myosin overlap
What happens to A band?- stays the same size; What happens to I-band and H zone?- both get smaller and disappear at full contraction

Theory:
-sarcomere shorten during contraction because myosin forms cross-bridges to pull along actin
-actin is anchored to the z disks; pulling on actin results in shortening of the sarcomere and contraction of the muscle
*sarcomeres need to all contract simultaneously for muscle contraction to occur!*

Front 11

Steps in Sliding-Filament Theory

Back 11

Supported by length-tension relationship for single muscle fiber:
1. tension drops to near 0 when there is no overlap between actin and myosin
2. tension is maximal when there is maximum overlap between actin and myosin (cross bridges are optimally aligned)
3. Shortening beyond optimal overlap results in reduced tension
-more difficult for cross bridges to form
-some binding between wrong filaments
(excessive contraction - generally only induced experimentally)
4. Very short sarcomere --> myosin bumps the z disk; prevents further shortening (reduced tension)
-only induced experimentally

Front 12

Cross-Bridge Chemistry

Back 12

*Attach, pull, detach*
1. Myosin is an ATPase to slowly release ADP + Pi (from ATP)
2. Myosin-ADP-Pi complex extends and binds weakly to actin (only 1 myosin head)
3. Pi released -> stronger actin-myosin bond forms
->chemical energy goes to kinetic energy
-> myosin head rotates producing mechanical force
4. ADP released and new ATP binds -> causes actin-myosin bond to weaken

Tradeoff: When one is contracting, the other is relaxing

Front 13

Isometric contraction

Back 13

length of muscle constant while force increases (cross-bridges repeatedly made and broken)- muscles work at maximal force when not moving -i.e. weight lifting

Front 14

Isotonic contraction

Back 14

muscle shortens while generating constant force (i.e. basic tension during aerobic exercise)

Front 15

Force-velocity relationship

Back 15

-as load increases, muscle velocity increases
-maximal force -> no velocity (isometric contraction)
-no force -> Vmax (lifting feathers v.s block)

Front 16

Power

Back 16

Power of muscle = work/time (force) x shortening velocity
-power is maximal at intermediate shortening velocity
-power = 0 if velocity=0 or force= 0
-power maximized if V/Vmax = 0.4 for most muscles

Front 17

Why does increased velocity = reduced force

Back 17

1. number of cross bridges formed decreases -> less positive force
2. More cross-bridges forming poor attachments
-> more negative force
-> at Vmax: # of neg. cross bridges = # of positive cross bridges (b/c no force)
- negative cross bridges formed when pushed too far

Front 18

Role of Ca2+ in the Regulation of Contraction

Back 18

-increased Ca2+ conc = increased force
-both Ca2+ and ATP needed for muscle contraction (only ATP needed for relaxation to replace ADP)
-Ca2+ interacts with tropomyosin and troponin:
-> relaxed fiber: tropomyosin blocks myosin binding site on actin
-> troponin is complex of 3 subunits:
1. troponin C: binds Ca2+
2. Troponin T: binds tropomyosin
3. Troponin I: binds actin and Troponin C
->Ca2+ binds troponin -> tropomyosin moves -> myosin binds actin

Front 19

Excitation-Contraction Coupling (in contraction)

Back 19

AP in fiber changes Ca2+ conc in the cytosol
-muscle fiber AP causes change in Vm: -90 mV to +50mV
-AP must be carried deep into the fiber to induce contraction of all myofibrils

Active State: increased stretch resistance following brief stimulation (bound cross-bridges)
Twitch: -brief increase in tension due to formation of actin-myosin bonds
-active stage rapidly terminated by removal of Ca2+ by pump
-not enough time to fully stretch elastic components
Tetanus: - next AP arrives before all Ca2+ is removed
-> Summation of contraction: multiple twitches fuse during high frequency stimulation
-elastic component does not return to slack position

*In order to get muscle contraction - need a lot of stimulation/Ca2+ flow*

Front 20

T Tubules

Back 20

hollow membrane tube at each z disk
-small pulses of current induce local contractions only if electrode is over z disk
-t tubule = link between plasma membrane and myofibrils deep in fiber

*T tubules carry the signal to the muscle fibers, when AP hits z disk, changes direction and enters the t tubule

Front 21

Sarcoplasmic reticulum

Back 21

intracellular membrane system; forms hollow collar around each myfibril (where Ca2+ is stored- good source!)
-derived from the endoplasmic reticulum (in the middle= glycogen)
-Ca2+ pumps actively transport Ca2+ into the SR
-Calsequestrin: Ca-binding protein within the SR; keeps free cytosolic Ca2+ conc. low
-AP conducted along T tubule induces the SR to release Ca2+ into the cytoplasm

Front 22

Receptors involved in regulation of contraction

Back 22

1. Ryanodine receptors: Ca2+ channel spanning SR membrane -> opening up is how Ca2+ is released
2. Dihydropyridine receptors:
-proteins in T tubule membrane
-voltage-gated Ca2+ channels; respond to APs
-little Ca2+ flows through the dihydropyridine channels (DHP); induce opening of ryanodine channels -> initially more Ca2+ extracellularly, so small amount of Ca2+ flows though
-when ryanodine channel opened- lots of Ca2+
-but SR= major source of Ca2+

Front 23

Plunger model

Back 23

1. Depolarized T tubule -> conformational change in DHP receptors
2. DHP channel is associated with ryanodine receptor -> opens Ca2+ channel
3. Ca2+ flows through ryanodine receptor from SR to cytosol

Front 24

Calcium-induced calcium release

Back 24

-50% of ryanodine receptors are not associated with DHP receptors
-open via voltage-gating due to increase in intracellular Ca2+ (positive feedback)

Front 25

Contraction-Relaxation Cycle

Back 25

1. Pre-synaptic AP leads to graded epp leads to AP in fiber (if reaches threshold)
2. AP travels down T tubule
3. DHP/ryanodine interaction
-> open Ca2+ channels in SR
-> Ca2+ flows into the cytosol
4. Vm returns to Vrest in t tubule
-> DHP channels deactivate
5. Ca2+ binds to troponin-> moves tropomyosin-> allows formation of actin-myosin cross-bridge
6. ATP->ADP causes myosin head to rotate, pulling on actin
-> leads to shortening of sarcomere
7. ATP binds myosin-> myosin detaches from actin
8. Ca2+ pumped back into the SR
-> Ca2+ release from troponin
->tropomyosin blocks cross-bridge formation
->muscle relaxes

Front 26

How is ATP produced during contraction?

Back 26

1. Anaerobic metabolism (glycolosis)
glucose-> 2 pyruvate + 2ATP + 2NADH
2. Aerobic metabolism
glucose + O2 -> H2O + CO2 + 38ATP

Front 27

What consumes ATP during muscle contraction?

Back 27

1. Myosin acts as ATPase (breaks down ATP-> ADP) during cross-bridge formation
2. Ca2+ pump (active transport)
-2 ATP/Ca2+ pumped into the SR
-25-50% of ATP used during muscle contraction

Front 28

Creatine Phosphate

Back 28

Second high-energy molecule (besides ATP) within muscle fibers
-creatine phosphokinase: transfers phosphate from phosphocreatine to ADP to produce ATP
-ATP buffer during short bursts of anaerobic muscle activity

*like a buffer- not used directly in oxidative phosphorylation, but storehouse to assist in ATP production*
-generally used in quick energy bursts

Front 29

Tonic Fibers

Back 29

-contract very slowly, do not produce twitches
-postural muscles of amphibians, reptiles, birds; muscle spindles that house stretch receptors
-no APs; neurons run along fiber forming multiple synapses- slow graded potentials so need many connections (why there are multiple synapses)

*limited in mammals (house stretch receptors)

Front 30

Slow twitch fibers (SO, type I)

Back 30

-contract and fatigue slowly; low Vmax
->many mitochondria, rich blood supply (red muscle)
-> use ATP slowly
-Mammalian postural muscles (take over job of tonic fibers in reptiles)
-Generate APs and twitches

Front 31

Fast-twitch oxidative (FOG, type IIa)

Back 31

-contract quickly and fatigue slowly
-high Vmax
-sustained, strenuous motion
-flight muscles of migratory birds
-many mitochondria (not as many as SO)
(endurance athletes- aerobic)

Front 32

Fast-twitch glycolytic (FG, type IIb)

Back 32

-contract and fatigue rapidly
-high Vmax
-few mitochondria
-rapid bursts motion
-i.e. breast muscles of domestic birds (chicken)

(sprinters)- anaerobic b/c does not use mitochondria

Front 33

Energetic Trade-off

Back 33

speed vs. metabolic cost
-more force generated by fibers with higher Vmax
-Higher Vmax - faster ATP use
-Fibers with lower Vmax are more efficient at low rates of shortening
-> Efficiency= power/energy used

-higher vmax= higher power and uses up more energy
-> also less efficient but efficiency varies based on what fibers are used for

Front 34

Vertebrate neural control of muscles

Back 34

1. Muscle arranged in antagonistic pairs
- flexor: closes joint (e.g. bicep, hamstring)
-Extensor: opens joint (e.g. triceps, quadriceps)
-alternate inhibitory and excitatory input- stimulation on one while relaxation on the other
(via interneurons from spinal column)
2. Neuron may innervate many fibers: each fiber receives input from one neuron
-Motor pool: all motor neurons that innervate a muscle; somata clustered in spinal cord (ventral horn) near muscle
-Motor unit: motor neuron and all fibers it innervates (~100 fibers)
-> smaller motor unit = more precise movement (axon acting on only a few fibers- i.e. in fingers)
-> more motor units activated = stronger contraction for particular muscle
-> single AP usually induces twitch in all fibers in motor unit

3. All vertebrate motor neurons are excitatory (neurotransmitter = acetylcholine)
-if you want muscle to relax- no signal sent (lack of stimulation)

Front 35

Cardiac Muscle

Back 35

1. Fibers = small elongate cells w/ single nucleus
2. Fibers connected by intercalated disks with gap junctions (electrical "synapse") b/w muscles
3. 2 major types
a. contractile fibers- striated with myofibrils
b. conducting fibers- don't contract, but transmit electrical signals (like nerves) i.e. pacemaker cells
4. Myogenic- contraction initiated by muscle- do not need neural stimulation
5. long AP w/ long refractory period
-> leads to regular predictable contractions and steady pumping

Front 36

Smooth Muscle

Back 36

1. fibers = small elongate cells with single nucleus
2. lack striations- bundles of actin and myosin- not anchored at z disks, but anchored at dense bodies (within cells) or attachment plaques (between cells)

--slow contraction regulated by extracellular Ca2+
-> Caldesmon: blocks actin-myosin binding (instead of tropomyosin)
-> Ca 2+ binds calmodulin -> binds caldesmon -> allows actin-myosin binding
3. No t tubules, under developed SR- no wrapping around actin/myosin

Front 37

Types of Smooth Muscle

Back 37

Single-unit: cells connected by gap junctions; myogenic (e.g., digestive organs, bladder, uterus)
-> similar to cardiac- does not require neural input to contract

Multi-unit: no gap junctions; neurogenic (e.g. blood vessel walls)- surround arteries

Front 38

Nervous vs. Endocrine in Intercellular communication

Back 38

Nervous:
Target= neurons, muscle fibers, and endocrine tissue (more specific)
-quick response (msec, sec)
-response is short in duration
-high level of voluntary control (somatic)

Endocrine:
Target = any cell in body
-slower response (min->days)
-long lasting response (-seasonal changes, dietary changes)
-little voluntary control

Front 39

Intercellular Communication

Back 39

1. Autocrine: affects the same cell that secreted it (i.e. sex steroids)
2. Paracrine: affect neighboring cells (i.e. neurotransmitters)
3. Endocrine: released into the bloodstream and act on distant tissues (e.g. hormones)
4. Exocrine: released onto body surface
-> mucus: thick fluid of mucin secreted by globlet cells
-> pheromones: communicate b.w animals (i.e. fire ants and moths secrete pheromones for signaling (swarm, mate))

Front 40

Signaling Molecules

Back 40

1. Hormone: chemical messenger released from cells into the bloodstream to exert action of target cells some distance away
2. Neurotransmitter: chemical messenger that acts across a neural synapse
3. Neurohormone: chemical messenger released by a neuron into the blood stream
a. neuropeptide: peptide hormone produced by a neuron
b. neurosteroid: steroid hormone produced by a neuron
4. Neuromodulator: hormone or neurotransmitter that modifies synaptic function

Front 41

Endocrine glands

Back 41

-ductless tissue
-rich blood supply
-distinct from exocrine glands (e.g. salivary, sweat)

*the endocrine system also has tissues with other major functions (e.g. gonads, brain, kidney, digestive organs)

Front 42

Neurosecretory cells

Back 42

-neurons that secrete neurohormones into the blood
-AP causes hormone release
-e.g. oxytocin and ADH release from posterior pituitary
-integration b/w nevous and endocrine system! synapse attached onto blood vessle

Front 43

Role of Ca2+ in secretory mechanisms

Back 43

1. Depolarization at terminal of neurosecretory cell -> neurohormone release
2. Stimulation of endocrine cells -> elevated Ca2+ (from ER) -> exocytosis of hormone

Front 44

Protein Hormones

Back 44

-most hormones are proteins
-hydrophilic- cannot cross membrane
Steps in Synthesis of Peptide Hormone:
1. DNA->mRNA-> protein + preprohormone in RER
2. Signal peptide signals transport to Golgi
3. Signal peptide is cleaved, just prior to transfer from RER to Golgi-> produces prohormone
4. Further processing in Golgi and vesicles produce active hormone (inactive fragment is chopped off)- can also be cleaved after release if hormone is present

Front 45

Monoamines

Back 45

derived from single amino acid
-most are neurohormones
-example: catecholamines (epinephrine, norepinephrine, and dopamine)
-hydrophilic- need vesicles for transport

Front 46

Iodinated thyroid hormones

Back 46

-Triiodothryonine (T3) and thyroxine (T4) are tyrosine derivatives)
-have iodine residues
-hydrophobic

Front 47

Steroid Hormones

Back 47

-cholesterol derivatives produced by enzymes in mitochondria and cytoplasm
-secreted by:
a. adrenal glands (glucocorticoids and mineralcorticoids)
b. gonads (estrogens, androgens, progestins)
c. placenta (estrogens, progestins)
-hydrophobic

Front 48

Hydrophobic vs. Hydrophilic Hormones

Back 48

Hydrophilic:
1. Stored in vesicles
2. Regulated release: secreted by exocytosis in response to stimulus
3. transported dissolved in extracellular fluid
4. Transmembrane receptors
5. Rapid Effects

Hydrophobic:
1. Synthesized on demand
2. Constitutive release- diffuse out of cell at rate synthesized
3. transported bound to carrier proteins (binding globulins)
4. Intracellular receptors
5. Effects usually slower
-> receptor-hormone complex usually acts as a transcription factor

Front 49

Hormone Signaling Pathways

Back 49

Hormones activate multiple receptor types
-Divergent paths: lead to different effects
-Convergent paths: amplify the same effect

First messenger = hormone, neurohormone, or neurotransmitter

Second messenger = intracellular molecules that respond to receptor binding
examples:
cAMP -> catecholamines, glucagon, LH, FSH, TSH, calcitonin, PTH, ADH
cGMP -> ANP
Inositol phospholipids -> catecholamines, ADH, GnRH, TRH

Front 50

cAMP Pathway

Back 50

1. Hormone binds receptor -> either stimulatory or inhibitory (dictated by the receptor)
2. G-protein activated: alpha subunit binds GTP (inactivated when GTP->GDP)
3. G-protein activate or inhibit adenylate cyclase (membrane bound enzyme)
4. Adenylate cyclase converts ATP-> cAMP
5. cAMP activates protein kinase A (PKA)- also called cAMP dependent protein kinase -usually inactive due to regulatory subunit
6. PKA phosphorylates proteins
7. Final effects- enzyme activation, protein synthesis, muscle contraction, nerve stimulation, hormone release

*inhibitory effect coming in at the g-protein

Front 51

cAMP signal amplification pathway

Back 51

1. receptor activates many G-proteins
2. Adenylate cyclase converts many ATP to cAMP
3. PKA activates many effector molecules
4. Many effectors act as enzymes

*1 receptor being stimulated can have a master/dramatic effect on the cell!*

Front 52

Inositol phospholipid pathway

Back 52

1. Hormone binds receptor-> activate G-protein
2. G-protein activates phospholipase C (PLC) -> rather than adenylyl cyclase
3. PLC converts PIP2 to inositol triphosphate (IP3) and diacyl glycerol (DAG) (IP3 and DAG = major second messengers- take the place of cAMP)
4. IP3 increases extracellular Ca2+
5. DAG -> converts arachadonic acid to eicosanoids (paracrine and autocrine signaling- local effects)
-> with Ca2+ activates protein kinase C (PKC)

Front 53

Ca2+ pathways

Back 53

-Intracellular Ca2+ increased by opening of cell membrane channels or release from ER
-Calmodulin: binds 4 Ca2+ molecules (and becomes activated)
-> Ca2+/calmodulin complex activates numerous enzymes (i.e. adenylate cylcase, phospholipidases, etc.)
- thus very important for signaling in the cell!

Front 54

Steroid Hormone Pathway

Back 54

1. Steroid diffuses into the cell
2. Hormone binds receptor intracellularly, activating it -> release of heat shock proteins (hsp)
3. 2 Hormone receptor complexes coming together and bind to form homodimer
4. H-R complex binds to DNA at hormone-responsive element (HRE)
5. Many co-activators recruited to bind more tightly to DNA
6. Entire complex acts as a transcription factor (DNA-> RNA)

Front 55

Hypothalamus

Back 55

diencephalon; under the thalamus; lower portion of 3rd ventricle
-region of lower brain that integrates endocrine and nervous function

Front 56

Tropic Hormones

Back 56

act on other endocrine tissue leading to the release of a hormone/ or can be inhibitory
-all are peptides except PIH (dopamine)

Front 57

Releasing Hormones

Back 57

Stimulate the anterior pituitary to secrete hormones
a. Corticoptropin-releasing hormone (CRH) -> ACTH release
b. GH-releasing hormone (GRH) -> GH release
c. Gonadotropin-releasing hormone (GnRH) -> FSH and LH release
d. TSH-releasing hormone (TRH) -> TSH release

Front 58

Inhibiting Hormones

Back 58

prevent the anterior and intermediate pituitary from secreting hormones
a. MSH-inhibiting hormone (MIH) -> inhibits MSH
b. Prolactin-Inhibiting Hormone (PIH= dopamine) -> inhibits prolactin
c. Somatostatin (GIH) -> inhibits GH, TSH, insulin, glucagon

Front 59

Neurohormones

Back 59

somata in hypothalamus; terminals release hormones in posterior pituitary
a. oxytocin
b. anti-diuretic hormone (ADH)

portal system in anterior pituitary -> veins that come together, branch out, then come together

Front 60

Tropic Hormones in Anterior Pituitary

Back 60

a. Adrenocorticotropic hormone (ACTH) -> secretion of corticosteroids by adrenal cortex
b. Gonadotropins (glycoproteins): -FSH ans LH
c. Thyroid-Stimulating Hormone (TSH)-> secretion of T3/T4

Front 61

Non Tropic Hormones in Anterior Pituitary

Back 61

Prolactin-> mammary gland development, milk production
Growth Hormone (GH)
*both promote cell division!*

Front 62

Growth Hormone Function

Back 62

Direct effects:
-stem cell division and differentiation in connective tissue
-lipolysis and glucneogenesis in adipose
-glucose metabolism

Indirect effects: stimulate release of somatomedins (IGF-1 and IGF-2) from the liver -> promote cell proliferation throughout the body

Front 63

Intermediate Pituitary

Back 63

-Melanocyte-stimulating hormone (MSH) -> melanin production in skin (color changes)
-humans lack intermediate pituitary: MSH produced by keratinocytes to have paracrine effects on melanocytes
i.e. rats in which cAMP pathway assoc. w/ MSH is stimulated creates sunless tan!

Front 64

Short-loop feedback

Back 64

hormone itself or direct effect of hormone is inhibitory

Front 65

Long-loop feedback

Back 65

multiple step feedback loop

Front 66

Posterior Pituitary

Back 66

release neurosecretory hormones produced by hypothalamus
1. oxytocin: stimulates contraction of the uterus and mammary glands: positive feedback loops
2. Antidiuretic hormone (ADH): promotes retention of water by the kidneys: elevates b.p (vasopressin)

Front 67

Adrenal Cortex Steroids

Back 67

Glucocorticoids (C21: cortisol in humans, corticosterone in rats)
-zona fasiculata
-raises blood glucose (liver- glycogen-> glucose)
-negative feedback with hypothalamus and pituitary (stops production of ACTH/CRH)

Mineralcorticoids (C21: aldosterone):
-zona glomerulosa
-promotes reabsorption of Na+ and excretion of K+ in kidneys
-secretion regulated by K+ in blood (increased K+ levels stimulates aldosterone and Na+ secreted into blood)

Androgens (C19)
-zona reticularis
-DHEA: maintains muscle tone; declines with age

Front 68

Adrenal Medulla Hormones

Back 68

Norepinephrine: mainly neurotransmitter of sympathetic
-some hormonal release from medulla

Epinephrine: -mainly hormonal release from medulla
-limited neurotransmitter in the brain

*stimulated by sympathetic nervous system- fight or flight stress response!*

Front 69

Adrenal Medulla

Back 69

inner portion (neural)
derived from ectodermal tissue
-pre-ganglionic neuron synapses onto adrenal medulla!

Front 70

Adrenal Cortex

Back 70

outer portion
derived from mesodermal tissue

Front 71

Adrenoceptors

Back 71

alpha1: E>NE, phosphatidal inositol pathway, function = vasoconstriction in digestive tract

alpha2: E> NE, inhibitory cAMP pathway, Functions = block beta receptor effects (neg. feedback), inhibits release of insulin (stress response), autoinhibitory on NE release (neg. feedback)

beta1: E=NE, excitatory cAMP pathway, functions = increased cardiac contraction (strength), increase carbohydrate + lipid catabolism (lipolysis/glycolysis- leads to increase circulating blood glucose), inhibits protein catabolism, stimulates glucagon

beta2: E>NE, excitatory cAMP, functions = bronchiodilation (increased lung volume), vasodilation, increased circulation to muscles

*IN GENERAL- more B than a receptors, but a-receptor effects usually greater than B-receptor effects*

Front 72

Thyroid gland

Back 72

2 lobes on trachea
1. T3 and T4
-T3 functions: elevated glucose metabolism (thermogenesis), maintain growth: priming effect for GH (surge in T3 during growth phase), regulate metamorphosis in amphibians
-neg. feedback of T4 on TSH
-lipid-soluble: acts through gene transcription

i.e. paedormorphosis in salamander: retaining juvenile characteristics into adulthood- in this case- due to lack of T3

2. Calcitonin:
-lowers blood Ca2+ levels, high Ca2+-> increased secretion, low Ca2+-> decreased secretion

Front 73

Parathyroid glands

Back 73

4 glands embedded in thyroid
-parathyroid hormone (PTH): raises blood Ca2+ levels, high Ca2+-> decreased secretion, low Ca2+-> increase secretion

Front 74

Pancreas

Back 74

hormones that regulate blood sugar levels
1. Insulin: lowers blood glucose levels
-produced in B cells in islets of langerhans
-stimulates all body cells (except CNS) to take up glucose
-stimulates liver to convert glucose to glycogen for storage
Type 1 Diabetes: loss of B cells, autoimmune
Type 2 Diabetes: Defective signal reception by insulin receptors

2. Glucagon: raises blood sugar levels
-produced in a-cells in islets of langerhans
-stimulates liver to break down glycogen into glucose

Front 75

Testes

Back 75

-FSH- spermatogenesis in sertoli cells
-sertoli cells release inhibin (neg. feedback)
-LH-> androgen production in Leydig cells
-androgens (c19 steroids): spermatogenesis, male secondary sex characteristics, behavioral effects

Front 76

Ovaries

Back 76

LH- thecal cell production of androgens
FSH- follicle maturation; aromatization of androgens to estrogens
-Estrogens (C18 steroids): corpus lutea formation, female secondary sex characteristics, water retention, bone mineralization

*testosterone produced in the ovaries first! then converted to estrogens*

Front 77

Ovarian Cycle

Back 77

ova development and ovulation
1. Follicular Phase: Several ovarian follicles begin to grow. One follicle becomes dominant
2. Ovulation: Follicle and adjacent wall of the ovary rupture: secondary oocyte is released (due to pressure buildup)
3. Luteal phase: corpus luteum develops (high intracellular cholesterol)- produces estradiol and proesterone

Front 78

Hormonal Female reproductive cycle

Back 78

1. Follicular Phase:
-GnRH- stimulates secretion of small amounts of FSH and LH
-LH- thecal cell production of androgens
-FSH- follicle maturation and aromatization
-Estradiol- inhibits FSH and LH, stimulates endometrial (wall of uterus) thickening
-neg. feedback effect
2. Ovulation: estradiol above a critical level for 36 hours -> elevated GnRH-> LH surge -> ovulation
3. Luteal Phase:
-LH-> granulosa cell maturation into the corpus luteum
-corpus luteum-> progesterone production
progesterone-> inhibits GnRH, reduces LH and FSH
4. No implantation:
-corpus luteum disintegrates-> reduced progesterone and estradoil-> menstruation
-FSH rises-> new follicular phase
5. Successful Implantation (Blastocyst)
-Embryo secretes human chorionic gonadotropin (HCG) -> maintains corpus luteum and endometrium-> no menstruation
-placenta begins producing estradiol and progesterone

Front 79

What are the functions of the circulatory system?

Back 79

1. Transport of O2 and nutrients to tissue
2. Removing metabolic wastes from tissues (CO2)
3. Transport of hormones and other signaling molecules
4. Thermoregulation- distributing heat
5. Immune function- circulate antibodies and white blood cells

Front 80

Components of closed circulatory system

Back 80

1. Blood- circulatory fluid transports dissolved molecules and blood cells
2. Blood vessels
a. arteries- carry blood from hear to tissue
b. arterioles- small branches of arteries just prior to capillaries
c. capillaries- thin-walled site of chemical exchange with tissues
d. venules- small branches of veins after capillaries
e. carry blood from tissue to the heart
3. Heart- muscular pump
a. atria- chamber that collect the blood
b. ventricles- chambers that pump blood out of the heart

Front 81

Open Circulatory System

Back 81

Hemolymph is pumped into fluid-filling hemocoel and bathes organs directly- "sloshing around of blood"
-most invertebrates
-arthropods have tracheal system to supply organs with oxygen

Front 82

Closed Circulatory System

Back 82

-blood flows in continuous circuit
-thin-walled capillaries allow transport of molecules
-blood is distinct from the interstitial fluid-> not in the case of invertebrates
-Lymphatic System: collects fluid from interstitial spaces and returns it to the circulatory system
-Annelids, cephalopods, and chordates
-vertebrates evolved a closed C.S from an open C.S. -> predatory lifestyle motivated evolution of closed C.S

Front 83

Evolution of Chordate Circulatory System

Back 83

1. Tunica intima
-inner layer of endothelial cells and elastic fibers
-homologous with endocardium
2. Tunica media
-middle layer of smooth muscle
-homologous with myocardium
3. Tunica adventitia
-fibrous outer coat
-homologous with epicardium

*Heart evolved from an artery!*

Front 84

Circulatory System of Chondrichthyes and Osteichthyes (shark)

Back 84

-4 chamber in series: sinus venosus-> atrium-> ventricle-> bulbus
-single circuit
-> high pressure in the gills
-> low pressure in systemic capillaries
-Single pressure heart

*ventricle still the same muscular pump like verts!- but only a single circuit so slower travelling of blood due to single pressure circuit*

Front 85

Circulatory System of Lungfish

Back 85

*Evolution of a double circuit!*

-3 chambers in series: atrium-> ventricle-> bulbus cordis; septum partially divides atrium and ventricle to separate oxygenated (systemic circuit-tissues) /de-oxygenated blood (gills-pulmonary)
-Double circulation: pulmonary and systemic
-> deoxygenated blood passes through gills and lungs
-> Ductus arteriosis: shunt bypass lungs
-Single pressure heart

*increased efficiency!- does not need to pass through gills to go to tissues*

Front 86

Circulatory System of an Amphibian

Back 86

-3 chambered heart (2 atria and 1 ventricle)
-Double circulation
-> deoxygenated blood directed toward pulmonary circuit
->oxygenated blood directed toward systematic circuit
-Single pressure heart
-pulmocutaneous circuit b/c oxygen source is from the lungs and skin

Front 87

Circulatory System of non-crocodilian reptiles

Back 87

-3 chambered heart (2 atria and 1 ventricle
-ventricles partially divided by horizontal septum-> larger septum- increased efficiency in separating oxy/de-oxy blood
-double circulation
-single pressure heart

Front 88

Circulatory System of Crocodilians

Back 88

-4 chambered heart (2 atria, 2 ventricles)
-Double circulation
-Double Pressure Heart (for the 1st time!)
-Interaortic shunt for diving (valve that closes pathway of blood to the lungs- not breathing- no flow through pulmonary artery

-common ancestor w/ birds

Front 89

Circulatory System of Mammals and Birds

Back 89

convergent evolution- similar trait evolving in 2 distantly related groups

-4 chambered heart (2 atria and 2 ventricles)
-Double circulation
-Double pressure heart
-> left side: only oxygenated blood
-> right side: only deoxygenated blood
Vena cava- major collecting vessle coming from systemic tract going into the heart
Aorta- from left ventricle to systemic tract

Front 90

Evolution of Chordate Circulatory System

Back 90

1. Open system-> closed system
2. Vessels (arteries) -> pumping heart
3. Single circuit -> double circuit
4. Single pressure -> double pressure

*snowshoe hare able to inhabit harsher climates due to more efficient circulatory system

Front 91

Valves

Back 91

Atrioventricular (AV) valves: between the atria and ventricles
Semilunar valves: between ventricles and 2 points where blood exits the heart (aorta, pulmonary trunk)
-not as efficient as AV valves
-prevent backflow from aorta-> ventricle

Cordae tendinae- fibers that connect the AV valves to capillary muscle (1-way valve)- comes in but cannot come out

blood flows from areas of high pressure to areas of low pressure

Front 92

Cardiac Cycle

Back 92

1. Mid-diastole:
-semilunar valves closed
-AV valves open
-Higher pressure in veins causes blood to rush through atria into ventricles
2. Atria systole: remaining blood is ejected from the atria to ventricles
3. Early ventricular systole
-pressure in ventricles causes the AV valve to close
-isometric contraction
4. Late ventricular systole
-increased ventricular pressure causes semilunar valves to open
-isotonic contraction
-blood rushes into aorta and pulmonary trunk
5. Early ventricular diastole
-reduced ventricular pressure causes the semilunar valves to close
-isometric relaxation

Front 93

Pacemaker cells

Back 93

-set the pace of heart beat!
-Located at sinoatrial (SA) node: inner wall of right atrium (vestigial sinus venosus- like in shark)
-pacemaker potential: spontaneous cyclic depolarization; multiple Ca2+. Na+, and K+ chanels (graded that brings it to threshold-> then AP)
-latent pacemaker cells take over if SA node is damaged
-pacemaker potential-> AP carried throughout heart
-> depolarization = inward Na+; prolonged plateau = inward Ca2+ (acts as a refractory period when AP cannot occur and prevents heart from going into tetanus)
-> impulse from the SA node delayed (0.1 sec) at the AV node- IMPORTANT so that atria can empty before ventricles contract
-> Purkinje fibers: carry AP from the apex throughout the ventricles

Front 94

cardiac output

Back 94

volume of blood pumped per minute from a ventricle
-> cardiac output = (stroke volume) x (heart rate)
-> stroke volume: the amount of blood ejected from a ventricle per beat
= (end-diastolic volume)- (end-systolic volume)

end-diastolic volume = after ventricle expansion- muscles are relaxed
end-systolic volume = end ventricular contraction

Front 95

What determines end-diastolic volume?

Back 95

1. Distensibility of ventricle walls (elasticity)
2. Size of ventricles- vary b/w species
3. Venus filling pressure
4. Pressure from atrial contraction
5. Timing of filing (longer time -> more volume)

Front 96

What determines end-systolic volume

Back 96

1. Pressure of ventricles
2. Pressure in aorta and pulmonary trunk- pressure gradients
3. Timing of contraction

Front 97

Plasma

Back 97

liquid portion of blood (40-60% of volume)
-ions maintain pH- highly buffered
-proteins maintain osmotic pressure and viscosity
-antibodies combat infections
-also: clotting factors, hormones, metabolic wastes, some respiratory gases

Front 98

Blood Cells

Back 98

a. platelets: pieces of cells involved in clotting (thrombocytes)- start clotting effect
b. erythrocytes (red blood cells): most numerous cell type; contain hemoglobin-> more O2 to tissue but viscosity increases so more clotting
-hematocrit: volume of erythrocytes in blood
c. Leukocytes (white blood cells): fight off infection

Front 99

Production of new blood

Back 99

-erythrocytes circulate 3-4 months
-pluripotent stem cells: cells in marrow of bones; develop into erythrocytes and leukocytes
-increased oxygen in the blood-> decreased erythrocyte production = negative feedback loop

Front 100

Clotting Process

Back 100

1. Hemorrhage exposes collagen fibers
2. Platlets release ADP (paracrine signal)
-> become sticky-> form plug
3. cascade of coagulation factors (13 factors)
4. prothrombin converted to thrombin
5. thrombin acts as enzyme that converts fibrinogen-> fibrin
6. Fibrin/ platelets act as mesh to trap RBC

Hemophilia = defect in coagulation factor 8

Front 101

Immune Response

Back 101

B cells: develop into plasma cells and secrete antibodies
Th cells (helper T cells): recognize antigen-> secretes cytokines (signaling factor in blood)-> promotes growth of Tc cells, B cells and macrophages
Tc cells (cytotoxic cells): recognize tumor cells-> develop cytotoxic T lymphocytes -> destroy tumor
Macrophages: endocytosis of cells marked with antibodies

Front 102

Hemodynamics

Back 102

1. Velocity of blood flow is inversely proportional to the cross-sectional area of the vessels
-slowest flow in capillaries: allows exchange between blood and tissue
2. Blood flows from high pressure to low pressure
-pressure is highest at aorta and lowest at vena cava (b/c pressure is coming from ventricles)
-law of bulk flow of fluids: Q = deltaP/R
R (resistance) = 8Ln/pi r^4
-Flow rate through straight vessels fits Poiselle's Law
Q = (P1-P2)pi r^4/ 8Ln
n=viscosity, Q= flow rate (vol/min)
*small change in r = large change in Q)
3. Laminar Flow: parabolic velocity profile of a fluid over a surface
-boundary layer near vessel walls does not flow- due to high resistance
-high viscosity of blood prevents turbulent flow
-higher hematocrit = higher viscosity
-Pulsatile flow occurs in larger arteries (backwash!)-i.e. aorta

veins= low pressure system- but valves help prevent backwash

Front 103

Artery Functions

Back 103

1. carry blood from heart to capillaries
2. elastic walls act as pressure reservoir
-damp pressure oscillations produced by heart beat
-anurism: ballooning of vessel; ruptured tunica adventitia
3. control distribution of blood to capillary beds
-constricting of arterioles redirect blood

Ventral = coming out of ventricles-> capillaries
Dorsal = minimal elasticity- more stable flow through capillaries

Front 104

Venus System

Back 104

-low pressure system: thin walled vessels
1. Blood loss-> decreased % venus volume
-smooth muscle of veins contract
-maintains arterial pressure and flow through capillaries
2. Skeletal muscle contraction assists in flow
-valves prevent reverse flow

Front 105

How does a Giraffe regulate blood flow when it raises and lowers its head?

Back 105

Raise: musculature of legs- less blood supply
-also, skin of giraffe is very tight so pushes blood back
-strong heart
-would otherwise lead to a big potential for edema in legs

Lower: series of valves in jugular vein, so when head is down, blood can still flow and won't go back to head

Front 106

What prevents a duck's foot from freezing on ice?

Back 106

-increased blood flow
*counter-current exchange- arteries and veins next to each other = heat gradient*