Regulation of Arterial Pressure Flashcards

1
Q
  • What is the equation for calculating MAP?
A

MAP=CO x TPR

or

MAP=HR x SV x TPR

or

MAP=2/3(DBP) + 1/3 (SBP)

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2
Q
  • Where are baroreceptors located?
  • What nerves are involved in each baroreceptor?
  • Where do they send their information?
A
  • Carotid sinus
    • CN 9 and Sinus nerve of Hering
  • Aortic sinus
    • Vagus (CN x) and Aortic nerve
  • BOTH send their information to NTS
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3
Q
  • What NTX do afferent signals from baroreceptors use when sending information to the NTS?
A

Glutamate

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4
Q
  • What are the mechanoreceptors most responsive to?
A
  • Rate of change in pressure rather than just the magnitude of change
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5
Q
  • What causes increased firing in a baroreceptor?
A
  • Increased stretch
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6
Q
  • What causes decreased firing in a baroreceptor?
A
  • Decreases in pressure/stretch
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7
Q
  • What area of the brainstem is involved in parasympathetic activity in CV function?
A
  • Dorsal motor nucleus of the vagus and nucleus ambiguus
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8
Q
  • What area of the brainstem is involved in sympathetic activity in CV function?
A
  • Rostral ventrolateral medulla
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9
Q
  • Stroke volume is dependent on ?
A
  • Sympathetic stimulation of the heart
  • Preload (EDV)
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10
Q
  • HR is dependent on?
A
  • Sympathetic stimulation
  • Parasympathetic stimulation
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11
Q
  • Total peripheral resistance (TPR) is dependent on?
A
  • Sympathetic stimulation of arterioles
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12
Q
  • What is the difference between aortic and carotid baroreceptors?
A
  • Aortic has higher threshold for activation
    • ​Continues to respond above saturation
    • Less sensitive to rate
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13
Q
  • Recruitment occurs up to _ mm Hg in carotid bodies
A

200

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14
Q
  • Low frequency of APs almost vanishes at _ mm Hg
A

40-60

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15
Q
  • Sympathetic nervous system causes _ baroreceptor firing rate
A

Decreased

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16
Q
  • What are the effects of the sympathetic nervous system on HR, contractility, vein and arteriolar radius, fluid retention?
A
  • Constriction of arterioles and veins (alpha receptors)
  • Increases HR and contractility (beta 1)
  • Renin secretion and increased fluid retention
17
Q
  • Parasympathetic nervous system causes _ baroreceptor firing rate
18
Q

What are the effects of the parasympathetic NS on arterial pressure?

A
  • We want to decrease MAP
  • Decrease HR
    • Vacus n signal to SA node
    • Muscarinic receptors
  • Also indirect vasodilation on blood vessels via NO
19
Q
  • What enzyme is secreted by the kidney in response to drops in BP? What type of cell secretes this?
A
  • Renin
  • Juxtaglomerular cells
20
Q
  • What stimulates the release of renin?
A
  • Sympathetic NS
  • *Specifically beta 1 adrenergic receptor activation*
21
Q
  • What does renin do as an enzyme?
A

Converts angiotensinogen to angiotensin I

22
Q
  • Angiotensin I is converted to Angiotensin II via which enzyme?
  • Where is this occurring?
23
Q
  • What does angiotensin II do in its active form?
A
  • Causes secretion of aldosterone from the adrenal cortex
  • Stimulates secretion of ADH/Vasopressin
  • Causes global constriction of arterioles by binding to AT1 receptors
24
Q
  • What does aldosterone do?
A
  • Increases Na+ and H2O retention
  • Increases blood volume, preload, SV, CO, and MAP
25
* What does ADH/Vasopressin do? * It is not only secreted in response to angiotensin II, but what other factors?
* **Acts on V1 and V2 receptors of smooth muscle, and collecting ducts, respectively and increases TPR and water retention** * Atrial receptors during low preload, increased osmolarity of blood
26
* What are the three natriuretic peptides that affect arterial pressure? * When are they secreted? * What are their effects?
* ANP, BNP, CNP * Excessive preload of atria and ventricles * Effects * **Arteriolar dilation-decrease TPR** * **Increases fluid loss-decreases preload** * **Inhibits renin-decreases TPR and preload**
27
* What happens when you have a hemorrhage?
* Decrease in blood volume and MAP * Decreased firing of mechanoreceptors * Increase sympathetic activation to bring MAP back up * Sympathetics will * Increase HR, CO and contractility via alpha ine adrenergic receptors * Constrict arterioles to increase TPR * Constrict the veins to decrease unstressed volume and increase venous return * Increased RAAS activation
28
* What happens when you have too much blood?
* Increase in blood volume and increase in MAP * Activate parasympathetics to bring MAP back down * Increased ANP secretion * Decreased ADH secretion * Renal vasodilation * Increased HR? (d/t increased preload?)\*
29
* What happens during exercise?
* Most important thing is getting blood to heart and skeletal muscle-increased sympathetic activation and decreased parasymp activation * Central command * **Increase HR/contractility via Beta 1 adrenergic receptors** * **Increase venous return** * **Alpha one receptor activation leads to SELECTIVE vasoconstriction in skin, kidney, splanchnic regions, and inactive muscle** * **Vasodilation in active muscles due to metabolites such as K+, adenosine and lactate** * **Effects:** * **​Increase in pulse pressure** * **SBP increases** * **DBP should not change much** * **Overall TPR will decrease (d/t dilation of skeletal muscle arterioles**
30
* What happens during orthostatic hypotension? * What happens in response?
* Decreased MAP; no change in HR and TPR, CO goes down from decreased venous return, central venous pressure decreases d/t pooling of blood in lower extremities * Increase sympathetic activation * Increase HR, contractility and CO via beta 1 adrenergic receptors * Want to increase TPR via constriction of arterioles * Want to decrease unstressed volume and increase venous return so we constrict the veins