Control of Circulation (B2: W3) Flashcards Preview

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Flashcards in Control of Circulation (B2: W3) Deck (46)

Aside from delivery of oxygen and removal of carbon dioxide, why do the tissues need blood flow?

  • Delivery of nutrients (glucose, amino acids, fatty acids, etc)
  • Removal of Hydrogen ions
  • Maintenance of proper concentration of other ions in the tissues
  • Transport of various hormones and other specific substances to different tissues


What is Ohm's law?

Q = P1 - P2/R 

Pressure differences/Resistance


Blood flows when pressur exceeds resistance


How do we find resistance using Poiseuille's Law?

R = 8nl/πr4



How are Ohm's law and Poiseuille's law combined to find the flow?

Q = ∆Pπr4/8nl

Q = ∆P/R (Ohm's)

R = 8nl/πr(Poiseuille's)



A change in which factor will have the greatest effect on changing the resistance?

The radius


What controls blood flow to a tissue?

Each tissue has the ability to control its own local bloow flow in proportion to its metabolic needs

  • The greater the metabolism in an organ, the greater its blood flow
  • Blood flow to each tissue is regulated as the minimum level that will supply its requirements


What are the body's regulatory mechanisms for controlling blood flow?

  • Adjustment of pump output in the heart 
  • Changes in diameter of resistance vessels
  • Alterations in the amount of blood pooled in the capacitance vessels - veins 
  • Changes in total extracellular fluid volume and its osmolality


What are the two mechanisms involved in the dual control of the peripheral circulation?

  • Local (Intrinsic) Mechanisms
  • Systemic (Extrinsic) Mechanisms


Of the two mechanisms involved in dual control of the circulation, which one is more important?

The relative importance of the two controls is not the same in all tissues

One or the other becomes more important in certain situations


What are local (intrinsic) mechanisms for control of the circulation?

  • Metabolic mechanisms
    • Release of vasodilators
    • Nutrient deficiency for vascular smooth muscle
  • Myogenic mechanisms
    • Sudden stretch
    • Reduced stretch

Pressure flow autoregulation

Active hyperemia

Reactive hyperemia


How does pressure flow autoregulation work?

Autoregulation is constant flow under varying pressures

Resistance must increase for this to happen


What is a possible mechanism (myogenic theory) for increased resistance in pressure flow autoregulation?

  • Arteriolar wall tension is the controlled variable in the vasculature
  • Suddent stretch of small blood vessels will cause the smooth muscle of the vessel wall to contract
    • Activation of stretch-activated cation Ca channels
  • Vascular smooth muscle contracts in response to an increase in pressure difference across the wall of a blood vessel


What happens to autoregulation of blood flow and vascular resistance as mean arterial pressure is altered?

This mechanism works within a range, but autoregulation cannot be maintained at extreme changes in mean arterial pressure

  • Safe range for blood flow is about 80-125% of normal
  • Arterial pressure of 60-160 mmHg 
    • Due to active adjustments of vascular resistance
  • Above 160 mmHg, vascular resistance decreases
  • Below 60 mmHg, vessels are fully dilated 


What is active hyperemia?

Increased blood flow caused by increased tissue activity

Ex: exercise - more tissue metabolism


What is reactive hyperemia?

Blood flow above control level upon release of an arterial occlusion


Occlusion of a blood vessel --> No blood flow

Release clamp --> pressure goes above normal

Ex: veins going to the heart


How can active hyperemia and reactive hyperemia be explained?

Best explained by the vasodilator metabolic theories 

  • Deficiency of O2 causes release of vasodilator substances
  • Increased metabolism causes release of vasodilator subtances
  • Deficiency of O2 and nutrients in the vascular smooth muscle inhibits the ability of the muscle to contract


The precise link between metabolism and blood flow is unknown. What are potential candidates for vasodilator metabolites?

  • CO2 (increase)
  • K
  • Adenosine
  • Increased osmolarity
  • Lactic acid 
  • PO4-
  • ATP
  • pH (decrease)
  • PgI2
  • O2 (decrease


What is the role of the vascular endothelium?

There is a functional interaction between endothelium and adjacent smooth muscle cells

  • Endothelium can be activated
  • Releases substances: EDRF (NO), PgI2 (prostaglandin), EDHF


What factors are involved in NO synthesis?

  • NOS (nitric oxide synthase)
  • iNOS (inducible NOS)
  • cNOS (constitutive NOS)

Synthesize NO

NO diffuses out of endothelial cell and into target cell



Why does vascular endothelium release EDRF (NO)?

  • Endothelium experiences shear stress associated with flow
  • With increased flow (and increased shear stress) endothelium releases factors - EDRF


What does EDRF (NO) do?


  • NO activates GC
  • Increases cGMP
  • Increases sequestering of intracelllar Ca
    • Less CA means less contraction
  • Velocity through vessels decreases


What are the systemic (extrinsic) mechanisms for controlling blood flow?

  • Humoral (hormonal)
    • Adrenal medullary hormones
    • RAAS
    • Endothelins 
    • Kinins
    • Natriuretic peptides
  • Neural 
    • Sympathetic (heart and blood vessels)
    • Parasympathetic (heart >> blood vessels) 


What is released upon stimulation of the adrenal glands?

Adrenal medullar hormones

  • Epinephrine (80%)
  • Norepinephrine (20%)

These hormones cause different reactions on different receptors in the body


What happens when alpha 1 receptors are stimulated?

  • Vasoconstriction
  • Increased peripheral resistance
  • Increased blood pressure


What happens when alpha 2 receptors are stimlated?

  • Inhibition of NE release
    • NE activates and inhibits its own release
    • Negative feedback
  • Vasoconstriction (veins>arteries)


What happens when ß1 receptors are stimulated sympathetically?

  • Tachycardia
  • Increased myocardial contracility 


What happens when ß2 receptors are stimulated sympathetically?

(In urinary bladder and some vascular smooth muscle)

  • Vasodilation
  • Slightly decreased peripheral resistance 


Which type of receptors does norepinephrine activate?

  • Alpha receptors (most VSM cells)
  • ß1 (heart)

NE is a really good neurotransmitter


Which type of receptors does Epinephrine activate?

  • ß1 (heart)
  • ß2 (some VSM cells)
  • Alpha receptors - much weaker activation

Epinephrine is not a great neurotransmitter


Which type of receptors does isoproterenol activate? (Not a hormone)

  • ß1 (some VSM cells)
  • ß2 (heart) 


What effect does circulating (not local) epinephrine have on cardiac output, systemic vascular resistance, and arterial blood pressure?

  • Increases cardiac output - binds to ß1 receptors in heart
    • Increases HR
  • Decreases vascular resistance - binds to ß2 in vascular smooth muscle cells
  • Increased systolic pressure, decreased diastolic pressure - greater stroke volume, less resistance


What effect does circulating (not local) norepinephrine have on cardiac ouptut, sytemic vascular resistance, and arterial blood pressure?

  • Cardiac output is uneffected 
    • HR goes down (vagal input)
  • Increases systemic vasuclar resistance - alpha stimulation 
  • Increases systolic and diastolic pressures 


What are endothelins?

Proteins released from the endothelium - cause vasoconstriction

  • Vasoconstriciton (veins > arteries)
  • Initially depresses BP (release of Pgl2) followed by increase in BP due to vasoconstriction
  • Positive inotropic and chronotropic effect
  • Increase plasma levels of ANP, renin, aldosterone, and catecholamines
  • Increase release of sympathetic transmitters
  • Produce brochoconstriction
  • Decrease glomerular filtration rate, renal blood flow, increases Na reabsorption


How does the renin-angiotensin-aldosteron mechanism in the kidneys affect blood pressure?

  • When systemic BP is low, renin is released from kidney
    • Converts angiotensinogen to angiotensin I
  • Angiotensin I becomes Angiotensin II
    • Tells the brain to release ADH
    • Tells adrenal glands to release aldosteron
  • Vasoconstriction and water retention
    • Decrease in Na excretion
    • Decrease in water excretion


Which group of kinins is degraded by kininase II into inactive fragments?

Bradykinin and lysylbradykinin



Kininase II is the same protein as angiotensin converting enzyme (ACE). What is the effect of ACE inhibitors?

Inhibit angiontensin II (vasoconstriction), thus lowering BP

Also will stop the degradation of bradykinin and lysylbradykinin (which cause vasodilation)


What  is ANP and where is it found?

Peptide that is synthesized, stored, and released by atrial myocytes in response to atrial distension

  • Found during hypervolemic states and congestive heart failure
  • Causes relaxation and vasodilation


Where is CNP found?

Human brain and vascular endothelium


Where is BNP and when is it released?

Found in the human heart and blood (not in the brain)

Found during hypervolemic states and congestive heart failure 



What is the function of natriuretic peptides as a whole?

This system serves as a counter-regulatory system for the RAAS

  1. Vasodilation
  2. Renal effects that lead to natriuresis and diuresis

Leads to

  • Decreased blood volume
  • Decreased arterial pressure
  • Decreased central venous pressure
  • Decreased pulmonary capillary wedge pressure
  • Decreased cardiac output


What major variables are influenced by sympathetic autonomic stimulation?

  • Peripheral vascular resistance
  • Heart rate
  • Contractile force of the heart
  • Venous tone


What is the relationship between the sympathetic neuronal control and the hormonal neuronal control?

  • Increase peripheral vascular resistance → increase mean arterial pressure
  • Increase HR → increase cardiac output
  • Increase contractile force → increase stroke volume
  • Increase venous tone → increase venous return 

Know this loop


What is the main factor that plays a central role in the excitation-contraction coupling in vascular smooth muscle?



What are the intracellular signal transduction mechanisms of vasoconstriction?

  • Activation of G protein coupled receptors
    • Activation of PLC: PIP2 → IP3 + DAG
    • Activation of PKC → release of Ca
    • Activation of MLCK and phosphorylation of myosin = contraction
  • Inhibition of Adenylyl Cyclase
    • Decrease in cAMP
    • Decrease in PKA
    • Increase in Ca


What are the intracellular signal transduction mechanisms of vasodilation?

  • Gs protein coupled activation of adenylyl cyclase
    • Incrase in cAMP
    • Increase in PKA
    • Decrease in calcium → relaxation
  • Gs coupled activation of guanylyl cyclase (also involves NO)
    • Increase in cGMP
    • Increase in PKG
    • Inhibits calcium → relaxation


Inhibiting the mechanisms for vasodilation will cause vasoconstriction, and vice versa. Which pathways need to be activated for each?

  • Vasoconstriction
    • Rec/PLC/IP3, DAG
    • Inhibit for vasodilation
  • Vasodilation
    • AC/cAMP/PKA
    • GC/cGMP/PKG
    • Inhibit for vasoconstriction