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Physiology > Control of Circulation (B2: W3) > Flashcards

Control of Circulation (B2: W3) Flashcards

1
Q

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

A
  • 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
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2
Q

What is Ohm’s law?

A

Q = P1 - P2/R

Pressure differences/Resistance

Blood flows when pressur exceeds resistance

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3
Q

How do we find resistance using Poiseuille’s Law?

A

R = 8nl/πr4

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4
Q

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

A

Q = ∆Pπr4/8nl

Q = ∆P/R (Ohm’s)

R = 8nl/πr4(Poiseuille’s)

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5
Q

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

A

The radius

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6
Q

What controls blood flow to a tissue?

A

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
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7
Q

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

A
  • 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
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8
Q

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

A
  • Local (Intrinsic) Mechanisms
  • Systemic (Extrinsic) Mechanisms
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9
Q

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

A

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

One or the other becomes more important in certain situations

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10
Q

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

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

  • Pressure flow autoregulation*
  • Active hyperemia*
  • Reactive hyperemia*
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11
Q

How does pressure flow autoregulation work?

A

Autoregulation is constant flow under varying pressures

Resistance must increase for this to happen

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12
Q

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

A
  • 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
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13
Q

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

A

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
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14
Q

What is active hyperemia?

A

Increased blood flow caused by increased tissue activity

Ex: exercise - more tissue metabolism

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15
Q

What is reactive hyperemia?

A

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

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16
Q

How can active hyperemia and reactive hyperemia be explained?

A

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
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17
Q

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

A
  • CO2 (increase)
  • K
  • Adenosine
  • Increased osmolarity
  • Lactic acid
  • PO4-
  • ATP
  • pH (decrease)
  • PgI2
  • O2 (decrease
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18
Q

What is the role of the vascular endothelium?

A

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

  • Endothelium can be activated
  • Releases substances: EDRF (NO), PgI2 (prostaglandin), EDHF
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19
Q

What factors are involved in NO synthesis?

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

Synthesize NO

NO diffuses out of endothelial cell and into target cell

20
Q

Why does vascular endothelium release EDRF (NO)?

A
  • Endothelium experiences shear stress associated with flow
  • With increased flow (and increased shear stress) endothelium releases factors - EDRF
21
Q

What does EDRF (NO) do?

A

Dilation!!

  • NO activates GC
  • Increases cGMP
  • Increases sequestering of intracelllar Ca
    • Less CA means less contraction
  • Velocity through vessels decreases
22
Q

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

A
  • Humoral (hormonal)
    • Adrenal medullary hormones
    • RAAS
    • Endothelins
    • Kinins
    • Natriuretic peptides
  • Neural
    • Sympathetic (heart and blood vessels)
    • Parasympathetic (heart >> blood vessels)
23
Q

What is released upon stimulation of the adrenal glands?

A

Adrenal medullar hormones

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

These hormones cause different reactions on different receptors in the body

24
Q

What happens when alpha 1 receptors are stimulated?

A
  • Vasoconstriction
  • Increased peripheral resistance
  • Increased blood pressure
25
Q

What happens when alpha 2 receptors are stimlated?

A
  • Inhibition of NE release
    • NE activates and inhibits its own release
    • Negative feedback
  • Vasoconstriction (veins>arteries)
26
Q

What happens when ß1 receptors are stimulated sympathetically?

A
  • Tachycardia
  • Increased myocardial contracility
27
Q

What happens when ß2 receptors are stimulated sympathetically?

A

(In urinary bladder and some vascular smooth muscle)

  • Vasodilation
  • Slightly decreased peripheral resistance
28
Q

Which type of receptors does norepinephrine activate?

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

NE is a really good neurotransmitter

29
Q

Which type of receptors does Epinephrine activate?

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

Epinephrine is not a great neurotransmitter

30
Q

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

A
  • ß1 (some VSM cells)
  • ß2 (heart)
31
Q

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

A
  • 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
32
Q

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

A
  • Cardiac output is uneffected
    • HR goes down (vagal input)
  • Increases systemic vasuclar resistance - alpha stimulation
  • Increases systolic and diastolic pressures
33
Q

What are endothelins?

A

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
34
Q

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

A
  • 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
35
Q

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

A

Bradykinin and lysylbradykinin

(vasodilation)

36
Q

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

A

Inhibit angiontensin II (vasoconstriction), thus lowering BP

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

37
Q

What is ANP and where is it found?

A

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
38
Q

Where is CNP found?

A

Human brain and vascular endothelium

39
Q

Where is BNP and when is it released?

A

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

Found during hypervolemic states and congestive heart failure

40
Q

What is the function of natriuretic peptides as a whole?

A

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
41
Q

What major variables are influenced by sympathetic autonomic stimulation?

A
  • Peripheral vascular resistance
  • Heart rate
  • Contractile force of the heart
  • Venous tone
42
Q

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

A
  • 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

43
Q

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

A

Calcium

44
Q

What are the intracellular signal transduction mechanisms of vasoconstriction?

A
  • 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
45
Q

What are the intracellular signal transduction mechanisms of vasodilation?

A
  • 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
46
Q

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

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

Physiology (29 decks)

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