Physiology 33,34,35 General Control Of Flow

Front 1

What makes of the walls of arterioles? and what do they respond to?

Back 1

these are lined by smooth muscles cells, and very little elastin

they respond to SNS innervation,
and metabolic and endocrine factors

Front 2

What is Basal tone?

Back 2

this is state of partial contraction, independent of metabolic and neural mechanism (based on intrinsic properties of the vessel)

Front 3

What is the Resting State?

Back 3

this a small bit of constriction (more so than basal tone), due to tonic sympathetic activity

Front 4

What general things result in active vasoconstriction

Back 4

sympathetic stimulation or constrictor hormones/metabolites

Front 5

what general things result in active vasodilation?

Back 5

dilator nerves, hormones, or local factors

Front 6

what general things result in passive vasoconstriction?

Back 6

this is the return to a normal state, from a dilated state...due to the removal of active dilator influences

Front 7

What is the consequence of vasoconstriction? what factors cause vasoconstiction?

Back 7

This leads to increased resistance, and decreased flow through the vessel. Casued by:

Myogenic activity
increased O2
Decreased Co2/metabolites
High endothelin
High Sympathic tone
Vasopressin, angiotensin 2

Front 8

What is the consequence of vasodilation? what factors cause vasodilation?

Back 8

This lowers resistance, and increases flow through the vessel

Caused by:
decreased myogenic activity
decreased O2
increased CO2 and metabolites
Increased NO
a decrease in sympathetic stimulation

histamine/heat

Front 9

What is active hyperemia?

Back 9

this is an increase in blood flow, due to an increase in Oxygen Consumption.

caused by: an accumlation of local metabolites, low O2, and high CO2
(metabolites: K+, PO4, prostoglandins, lactic acid, H+, adenosine, NO)

Front 10

Do veins respond to metabolic vasodilators?

Back 10

no they do not

Front 11

what is reactive hyperemia?

Back 11

this occurs when blood supply is occluded. The arterioles dilate due to:

-myogenic relaxation
- the same metabolic changes as in active hyperemia. results in far higher blood flow after the occlusion

Front 12

what is the magnitude and duration of the hyperemic response proportional to?

Back 12

the duration of the occlusion

Front 13

What organs use autoregulation of blood flow?

Back 13

the heart, brain, kidneys, skeletal muscle

Front 14

how do autoregulating organs respond to a drop in blood pressure?

Back 14

there is a compensatory vasodilatory response. Lower resistance improves flow

(Q=delta P/R)

Front 15

What is the myogenic hypothesis?

Back 15

this says that blood vessels will contract in response a sudden increase in pressure to maintain blood flow (constant BF)

same for a sudden decrease in BP, the vessels will relax and decrease resistance

Front 16

What does Vassopressin do? where does it come from?

Back 16

this comes from the pituitary

acts as a vasoconstrictor
increases water retention

Front 17

what does Angiotensin 2 do?

Back 17

this comes from angiotensin 1

acts as a vasoconstrictor

Front 18

what does Atrial Natriuretic Peptide do? where does it come from?

Back 18

this is released from the atria

vasodilator

counteracts hypercolemia

Front 19

What do sympathetics do in skin? what receptors? (blood flow)

Back 19

This is vasoconstriction via Alpha-1

Front 20

what do sympathetics do in Muscle? what receptors?

Back 20

vasoconstriction via Alpha-1 (from SNS FIBERS)

OR

Vasodilation via epinephrine and Beta-2 receptors

Front 21

What do sympathetic adrenergic fibers do? what receptor do they use (NT? pre or post ganglionic?)? WHERE do they work?

Back 21

these use Alpha-1 receptors
(POSTGANGLIONIC- NE transmitter)

controls vascular resistance in Precapillary vessels. (normally does some constriction)

Front 22

What do sympathetic cholinergic fibers do? WHERE do they work? What receptor? What NT?

Back 22

these do vasodilation in skeletal muscle

precapillary vessels

ACH- is the NT

M3 receptor

Front 23

what do Parasympathetic Cholinergic Fibers work? what do they do? what NT? what receptor?

Back 23

These are vasodilator fibers in gentialia, cerebral, and coronary systems.

M3 receptor

NO NT- FIBER ACTION

Front 24

What does Angiotensin 2 do? What receptor does it use? what causes its release

Back 24

What causes Vasoconstriction

acts on smooth muscle AT1 receptors

release is stimulated by drop in MAP or extracellular volume

(stimulates thirst, vasopressin release, and vasoconstriction)

Front 25

What does Vasopressin do? what causes its release? What receptor does it use?

Back 25

this is a vasconstrictor

acts on V1 receptors

released by posterior pituitary in response to rising plasma osmolarity, or low BP

Front 26

What does Atrial Natriuretic Peptide do? what receptor does it use?

Back 26

This is released with atrial stretch. (stored in atrial myocytes)

its a Vasodilator, stimulates guanylyl cyclase

Front 27

What does Brain type Natriuretic peptide do?

Back 27

this is stored in ventricle myocytes

released in response to ventricular pressure or volume overload

vasodilator, stimulates guanylyl cyclase

Front 28

What does ANP do in the kidneys? in response to what?

Back 28

this results in vasodilation, and an increase in Na+ and H2O excretion.
Lowers TPR

ANP is secreted in response to increased ECF and atrial pressure

Front 29

What are the 2 main jobs of Epinephrine? Where do they work? what receptor do they use?

Back 29

Vascular Smooth muscle: Alpha 1/2 receptors- Vasoconstriction

Skeletal Muscle: Vasodilation B2 receptors (due to high concentration of B2 receptors in SM, and high affinity for epi)

Front 30

What does NO do? (mechanism)

What releases NO, what causes its release?

Back 30

This is released by endothelial cells, this is stimulated by shear-stress (flow induced) (or other things that increase intracellular calcium)

NO diffuses into smooth muscle, activating Guanylyl Cyclase- Increases intracellular cGMP, relaxing smooth muscle

Front 31

What does Endothelium-derived Hyperpolarizing factor do?

Back 31

this hyperpolarizes smooth muscle, and leads to relaxation

Front 32

What does Prostacyclin do? what causes its release?

Back 32

this is released by endothelial cells, caused by shear stress

Increases intracellular cAMP

Leads to vascular smooth muscle relaxation

Front 33

What does Endothelin do? what receptor does it use?

Back 33

This is the most powerful vasoconstrictor known.

uses ET(a) receptor

released in response to stretching of blood vessels

Front 34

What do Prostaglandins do? What produces them?

Back 34

these are produced by aggregating platelets (thromboxane A2)

these induce vasoconstriction

Front 35

what do Kinins do?

Back 35

these cause venous contraction (either direct or prostaglandin mediated)

Front 36

What does Histamine do? What receptors does it act on?

Back 36

this is released by mast cells.

relaxes arterioles, and increases capillary permeability

H1 receptors on endothelial cells- NO release

H2 receptors on Smooth Muscle- cAMP content (vasodilation)

also stimulates PGI2 release

Front 37

What do capillary pores permit the passage of?

Back 37

small water-soluble substances

Front 38

what do capillaries branch from?

Back 38

either arterioles or metarterioles

Front 39

What contain precapillary sphincters?

Back 39

metarterioles

Front 40

What acts on precapillary sphincters?

Back 40

Only local metabolites, no innervation

Front 41

What is the plasma-colloid osmotic pressure? (Pi P)

Back 41

this is the force caused by plasma proteins, encourages fluid movement into capillary

Front 42

What are the forces that force fluid out of capillaries?

Back 42

Capillary blood pressure (Pc)

Interstitial Fluid Colloid Osmotic Pressure (Pi if)

Front 43

What are the forces that pressure fluid into capillaries?

Back 43

Plasma Colloid Osmotic Pressure

Intersistial Fluid Hydrostatic Pressure (very small force typically)

Front 44

What is the Net Exchange Pressure formula?

Back 44

NEP= (Capillary Pressure+ Interstitial fluid osmotic draw)- (Capillary osmotic draw+ Interstitial fluid pressure)

Front 45

why is bulk flow important?

Back 45

it proves extra fluid volume during a hemorrhage (fluid flows from Interstitial fluid into capillary)

Front 46

Where is extra interstitial fluid taken up?

Back 46

this is taken up by lymphatics

Front 47

How are the cells arranged in a lymph vessel?

Back 47

these are used arranged in layers that function as flaps, only allowing fluid to flow inwards

Front 48

What are the functions of lymph?

Back 48

this is one way network of return vessels. brings fluid back to the blood.

returns filtered fluid
immunity
transport of absorbed fats
returns filtered protein

Front 49

Whats the average daily lymph flow?

Back 49

about 3/L per day

Front 50

What 4 conditions can result in edema?

Back 50

Reduced plasma proteins (reduces inward draw back to veins)

Increased permeability of capillary walls (allows protein escape, IE histamine)

Increased Venous Pressure
(restriction of venous return...damming)

Blockage of Lymphatic vessels (elephantasis)

Front 51

What 4 things enhance venous return to the heart?

Back 51

Cardiac Output (generates pressure gradient)

Sympathetic induced Venoconstriction
(decreases venous capacity, elevates venous pressure)

Skeletal muscle pump, and venous valves

Respiration