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109 Cards in this Set

  • Front
  • Back
How is flow regulated at the whole body level
reflex control systems
How is flow regulated at the organ level
local control systems
Vasoactive substances
How much blood vessel is constricted or dilated
Types of Vasoactive Substances
Neurotransmitters (ANS effects)

Hormones (via circulation)

Local mediators (from endothelia or tissue)

Metabolites (O2, CO2, K+, adenosine)
Sympathetic Receptors
A1

B2

Ach
A1 sympathetic receptors
Locations: Arterioles in skin, muscle, kidney, splanchnic
Also veins

Effect: Constrict
For veins, constrict and reduce compliance
B2 sympathetic receptors
Location: Arterioles in skeletal muscle and arterioles

Effect: Dilate
Ach sympathetic receptors
Location: arterioles in skeletal muscle, skin? (palms, lips, soles)

Effect: Dilate
Parasympathetic Receptors
Ach

Bradykinin
Ach and Bradykinin parasympathetics receptors
Location: sweat glands, salivary glands, sex organs

Effect: dilate
Local/Endocrine Constrictors
From adrenal medulla, 8-% Epi & 20% NE
Types of Local/Endocrine Constrictors
Epi/NE via A1 receptors

angiotensin II

vasopressin

prostaglandin PGF2 A (potent smooth muscle constrictor)

thromboxane

endothelin
Epinephrine as endocrine constrictor
Epinephrine from adrenal medulla

FLIGHT OR FIGHT (sympathetic stimulation)
Vasopressin as endocrine constrictor
Vasopressin from posterior pituitary
Increased with dehydration, blood loss
Angiotensin II as endocrine constrictor
angiotensin II: product of renin-angiotensin system

Increased with dehydration, blood loss, sympathetic stimulation
Making Angiotensin II
Liver produces angiotensinogen

SNS to kidney produces Renin

Renin + Angiotensinogen form Angiotensin I

Angiotensin I + ACE in lungs (angiotensin converting enzyme) forms Angiotensin II
G Protein Coupled Aq receptors
IP3 interacts with RyR

Ca2+ causes constriction
Endocrines as local dilators
Epi/NE via B2 receptors (only in some places!)-skeletal muscle

Atrial natriuretic peptide
(ANP) - opp of ANG II

prostaglandin PGE2

prostacyclin

nitric oxide

also: CO2, lactic acid, other metabolites

adenosine
eNOS
Ca2+ dependent enzyme
G Coupled Protein Alpha S as a dilator
"big" K+ channels. Ca2+ activated. Spatially coupled to SR.

cAMP in, deactivates PLB that's on RyR. K+ out.

cGMP causes decrease in Ca2+, decrease in K+ (hyperpolarize). Effect is dilation
G Coupled Protein Alpha S as a Constrictor
"big" K+ channels. Ca2+ activated. Spatially coupled to SR

Ca2+ leaks out of SR - calveoli. IP3 in. Ca2+ binds to RyR. Ca2+ causes contriction
What determines tone with Alpha A
Balance of constriction and dilation
Local Control
Autoregulation: Intrinsic Control

mediated by LOCAL mediators of tone

This is the most important way blood flow is regulated in the heart and CNS

also important to renal function and with increased activity in muscle and skin
CONTROL OF THE CARDIOVASCULAR SYSTEM

Flow to organ
FLOW = Driving P/ R

(heart, brain flow determined by Pa, local Resistance)
Pa determined by CO and R elsewhere (TPR)
Shunting of flow
dilate to keep blood in brain

or increase driving pressure, increase cardiac output, increase resistance elswhere
No Autoregulation
No local control
Constance Resistance
With Autoregulation
Constant flow even though pressure has changed
Metabolic Control
Uses local vasodilators :
CO2, lactate, K+, low O2
(products of metabolism)

Match flow to metabolic needs
How this relates to flow?
Can increase pressure via shunting

Can increase flow to head during fight or flight

Can decrease resistance to gut after meal.
Variations in circulations
Neural Control VS Local Control??

Brain (cerebral)
Heart (coronary)
Kidney (renal)
Skin (cutaneous)
Skeletal muscle
GI tract (splanchnic)
Cerebral Circulation
Circle of Willis (internal carotid artery, middle cerebral artery, basilar artery)

One of few anasomoses in brain
Innervation of cerebral circulation
Sympathetic Nerves
Cholinergic Nerves
Sensory Nerves

Autoregulation over a range of -mmHg. Depends on O2, CO2, and adenosine
Sympathetic Nerves in Cerebral Circulation
NE, NPY - neuropeptide (constrict)

Lrg arteries
Cholinergic Nerves in Cerebral Circulation
Ach (NO formed), VIP - vasoactive intestinal peptide (dilate)

Lrg Arteries
Sensory Nerves is Cerebral Circulation
substance P, neurokinin, CGRP (dilate)
Cerebral Flow Regulated by Metabolites
Blood vessels in brains will vasodilate with low O2 or high CO2

Low PO2 then cerebral blood flow increases

Increase PCO2 in tissue then flow increase to get rid of CO2
Variations in Cerebral Blood FLow
Flow to areas changes with brain activity:

Local metabolic activity alters local flow!
Changes in cerebral blood flow with pathology
Seizures increase flow locally, decreased flow post seizure in area of focus

Alzheimer's disease decrease flow in superior parietal, then temporal, then frontal cortex
Also changes in Huntington’s, disease manic depression, schizophrenia

Also suggest flow linked to metabolic activity of neurons
Coronary circulation
Coronary artery branch from aorta near aortic valve
Large arteries travel on surface of heart,
Smaller arterioles must pass from epicardium to endocardium through contracting muscle
Coronary circulation - contraction
Contraction of heart compresses the arteries, so subendocardial flow only during diastole (mechanical property)

TACHYCARDIA decreases flow to left ventricle

Aortic stenosis decreases flow to left ventricle
Control of Coronary Circulation - Innervation
Innervation: minimal, but not zero. BC not many Alpha receptor in heart.

Direct α adrenergic constriction on VSM, but
β adrenergic receptors on HR, contractility lead to vasodilation via metabolic effects

Effects of nerve or NE- generally Vasodilation unless β-blocker
Control of Coronary Circulation - Autoregulation
Autoregulation critical and more important: Range 60-200 mmHg

Calibrates flow to O2 demand. Vasodilation produced by low O2, or high CO2, H+, K, lactate, prostaglandin, adenosine (Oxidative metabolism very important)

Reactive hyperemia present (increased flow after occlusion)
Renal Circulation
Innervation: sympathetics - very important

Regional autoregulation
Humoral factors can have local regional effects

In cases of severe renal vasoconstriction (hypovolemia) renal vasoconstriction can result in acute renal failure (ex-extreme dehydration)
Cutaneous circulation - Innervation and temperature response
Innervation : sympathetic, constrictor (Alpha)

Temperature response – shunting between arterial-venous anastomoses (unique to skin)
Cutaneous Circulation

Mechanical response and wheal
Mechanical response- contraction of precapillary sphincters

Wheal: vasodilation reflex from sensory neurons- substance P
Skeletal Muscle

Flow, Innervation
Able to increase flow by 20x with exercise - B2 dilation effect

Innervation: sympathetic A adrenergic can decrease flow to ¼ normal (precise use of sym)
Skeletal Muscle

Autoregulation, Mechanical Forces
Autoregulation: important in the exercising muscle, flow to contracting fibers increases as metabolism increases

BUT mechanical forces- compression of vessels can decrease flow in exercising muscle (downside)
GI Tract Circulation
Major regulation vs SNS
Contriction when body needs increase BP or flow to heart, brain
Dilation post-prandial

Autoregulation/metabolic effects : probably important in increasing flow to a given segment (eg stomach vs intestine) with digestion
Control of CV System
Variable sensed

Processing or Intergration

Response
Variable Sensed
Afferents
What is sensed? How? Where?

Pressure, volume, O2, CO2
Response
Efferents

What changes, How? Where?

Resistance, Rate, SV
Types of Sensory receptors
1. Baroreceptors
2. Atrail Receptors
3. Ventricular receptors
4. Central & Peripheral Chemoreceptors
5. Renal Baroreceptors
6. Osmoreceptors in hypothalamus
Baroreceptors
Stretch receptors in carotid sinus and aortic arch

Firing sends signal to brain: carotid BR via CN IX aortic BR via CN X (Vagus)

Can be reset
Atrial Receptors
At junction of great veins and atria

Type A fire with atrial contraction

Type B fire with increase venous return. "volume" receptors. Signal from vagus
Ventriculat Receptors
In wall of ventricle
Respond to stretch of ventricle with increased ventricular pressure.
Can cause reflex devrease heart rate

Aortic stenosis can activate
Central & Peripheral Chemoreceptors
In aortic arch & carotid sinus

respond to changes in O1 and CO2.
Help increase flow when aortic, carotid, or brain levels of O2 fall or CO2 rise
Renal Baroreceptors
Renin to ANG II

Respond to intrarenal perfusion pressure

Help maintain renal blood flow and blood volume
Osmoreceptors in Hypothalamus
Respond to NA+ concentration of ECF.

Cause AVP release and drinking (kidney retain volume)
Efferent Mechanisms can be
slow (hormonal) or fast (neural)
Sympathetic NS
Inc HR
Inc Contractility
Inc venous tone - less compliant (inc venous return)
Inc arteriolar resistance - esp to skin, GI, kidney.

Stimulate kidney renin to ANG II
Parasympathetic NS
Dec HR
Hormones Involved
epinephrine (adrenal)
AVP (pituitary)
renin-angiotensin- aldosterone (kidney-adrenal)

ACTH-cortisol (pituitary-adrenal), progesterone/estradiol
MAP equals
Cardiac Output x TPR (total resistance in systemic circulation)

CO equals SV x HR
Efferent:

Contractility
B1
Efferent:

Venous Compliance Return
A1
Efferent:

Volume
Longer term:

kidney, AVP, Ang II, Aldosterone
Efferent:

Dec Rate
Ach
Efferent:

Inc rate
B1
Efferent:

Vasoconstrict:
A1
AVP - if BP very low
ANG II
Efferent:

Vasodilate
B2
Role of arterial BR: What happens if arterial BP falls?
Dec BP leads to dec BR firing rate leads to change neuron firing in CNS

Dec Parasympathetic (VAGAL) - Inc HR

Inc Sympathetic firing to: arterioles (esp in GI tract, skin) - A1: Inc Resistance

heart: B1 - Inc HR

veins: A1 - Dec C
Result of Above reflex
Inc HR - Inc CO

Inc C - Inc SV and Inc CO

Inc Vasoconstriction - Inc R

Inc Venoconstriction (Dec Compliance) - Inc VR, Inc SV, Inc CO - Frank Starling Mech

Inc CO, Inc TPR, Inc BP toward normal
Dec in volume (Dec in BP) causes:
Dec BR firing rate
Dec afferent firing to MEDULLA

Dec Parasympathetic
Inc Sympathetic

Resistance increases

Compliance decreases

Contractility increases

Transcapillary fluid reabsorption increases
Dec in P in capillary if R in arterioles ince. Less fluid flows out.
What may happen at same time as reflexes?
At same time reflexes acting local effects may also be acting to change local vascular tone, esp in organs with good autoregulation
Inc BP causes:
Inc BR firing rate
Inc afferent firing to MEDULLA

Inc Parasympathetic (Dec HR)
Dec Sympathetic

Dec Resistance
Inc Compliance - keep more blood in veins, dec CO, Dec SV

Dec Contractility
Injection of Phenylephrine
A1 agonist - stimulates A1 receptors
VSM in arterioles cause vasocontriction
Inc BP & slows heart
Dec SV
Dec Contractility
Where is NO made?
In endothelial calls

Cause vasodilation

Dec BP
Atrial pressure and HR
As HR inc, Atrial pressure (systolic) Increases
Role of Atrial receptors: What happens if blood volume falls?
Dec VR
Dec Atrial B firing rate (susceptible to stretch)
change neuron firing to CNS (Dec BR firing)

Inc secretion of hormones vasopressin and renin-ang II - can help body to increase volume
Net effect of Fall in blood volume
increase retention of fluid
also increase vasoconstriction to SHUNT flow

Inc Sympathetic. A1 effect is vasoconstriction. B1 in kidney stimulates Renin
Effects of fluid intake - long term
Venous Return

Inc CO
Inc Arterial pressure
Inc to kidney urinary output
Effects of fluid intake - short term
Dec TPR
Dec CO
Inc Arterial pressure
Inc kidney output
Inc Arterial pressure
Increases:

HR
vasoconstriction
venoconstriction
contractility
Atherosclerosis
Form of arteriosclerosis caused by deposition of fat and fibrin over time

increases resistance (narrow vessles)
decreases flow to tissue
leads to complications: clotting, ischemia, etc
3 Steps of atherosclerosis
1. Fatty Streak
2. Fibrous Plaque
3. Complicated Lesion
Fatty Streak
Lipid deposition in intima and subintima
Fibrous Plaque
extends into lumen of vessel, also involves smooth muscle cells and tunica media
Complicated Lesion
alterations with time and local events: hemorrhage, cell necrosis, calcification, thrombosis
Etiology of Atherosclerosis
Hypertension: endothelial injury (“shear stress”)
Hyperlipidemia: LDL/HDL ratio
Oxidative damage: aging, diabetes
thrombogenesis and platelet activation

INFLAMMATORY DISEASE OF VESSEL WALL
Detailed fatty streak
lipid deposition in intima in foam cells

macrophages enter intima
adhesion (VCAMs)

take-up oxidized LDL lipids
oxidation of LDLs

LDL receptors “scavenger receptors”
Detailed fatty streak

cont
macrophages have fat. Normal intima does not have many macrophages

LDL gets into cells via VCAM

Oxidized LDL's get taken up first
Detailed Lesion Intiation
LDL oxidation
Oxidized LDL interact with matrix fibers

LDL trapped in matrix before getting taken up by macrophages
Detailed Fibrous Plaque
involves smooth muscle cells and fibrous tissue

Growth factors and cytokines from T-cells and macrophages induce SMC and matrix accumulation
Detailed Fibrous Plaque

cont
Cannot dilate and function as normal blood vessel. Can't regulate resistance

Cells that take up fate prone to necrosis. Clump together to necrotic core

Smooth muscle prob engulfs fat

Inc ANG II stimulates smooth muscle proliferation
Detailed Complicaed Lesion
necrosis, calcification, thrombosis

platelet aggregation (thromboxane A2 macrophages)

infection
Detailed Complicated Lesion

cont
Resistance further impaired

Luman and wall of vessel now invaded with Ca2+

Macrophages release thromboxane

Wall prone to infection
Complications associated with atheroslerosis
Increased blood pressure (hypertension) - cause or effect

decreased perfusion
(organ ischemia/damage; peripheral tissue ischemia/damage)

increased risk of thrombosus
(“stroke”)
Signs/Symptoms/Complications
ischemia- pain

fatigue (esp muscle fatigue)

intermittent claudication

thrombosis/embolism

hypertension
Ischmia
Restriction in blood supply
Intermittent Claudication
"limping"; cramplike pains in legs due to poor perfusion
Arteriosclerosis Obliterans
Plaques with complications

progressive stenosis and obstruction with atherosclerotic plaques

in medium and large sized arteries - esp to limbs

inadequate flow to tissues, results in pain, fatique, claudication
Signs/Symptoms
bruits - mumur in bv due to turbulent flow

reduction or loss of pulses below site of stenosis

if severe: muscle atrophy, cyanotic (Blue) discoloration, hair loss, gangrene, necrosis
Thrombosis
intrinsic pathway activated by blood pooling (aneurysms, obstructions), hypotension

extrinsic pathway activated by infection
Diseases associated with thrombosus
atherosclerosis‑disruption of intima starts clotting cascade

aneurysms‑ pooling of blood

infection‑invasion of intima

on cardiac valves‑ by calcification or bacterial infection (endocarditis)
Complications of Thrombosus
disseminated intravascular coagulopathy

thromboembolism

thrombophlebitis
disseminated intravascular coagulopathy
Very Bad! Activates and deactivatesd clotting cascade. Backa nd forth with excessive clotting and internal bleeding.

-childbirth or accident

High fatility rate. Once time episode
thromboembolism
Clot breaks and problems ensue
thrombophlebitis
Clot in vein. Want it to stay away from heart and lungs
A lot of pain involved.
Signs/Symptoms/Complications of Thrombosis
ischemia
(obstruction)‑PAIN

tenderness, swelling ( - Inc R = Inc hydrostatic press = fluid leaking out)

if arterial‑ skin pale (downstream)

if venous‑ skin red to deep blue‑purple

neuralgia‑ with edema(venous) - edema presses on nerves and causes pain

Embolism‑organ disruption, necrosis, sepsis