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Physiology Part 1 > Lec 13 Regulation of BP > Flashcards

Lec 13 Regulation of BP Flashcards

1
Q

How can we rearrange Ohms low for physiology?

A 
MAP = CO * TPR
MAP = mean arterial pressure
CO = cardiac output
TPR = total peripheral resistance
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2
Q

What does an increase in MAP do to CO?

A

nothing! – it is a one way causal relationship

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3
Q

What does increase in CO do to MAP?

A

increase in CO causes increase in MAP

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4
Q

What does increase in TPR do to MAP?

A

increase in TPR causes increase in MAP

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5
Q

What is equation for MAP [from DP and SP]?

A

MAP = 2/3 DP + 1/3 SP

because diastole lasts longer than systole

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6
Q

does systole or diastole last longer?

A

diastole twice as long as SP at rest

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7
Q

Where are baroreceptors? Function?

A
  • located in carotid sinus [mostly] and aortic arch

- initiate rapid response to changes in BP

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8
Q

What is function of atrial volume receptors?

A
  • respond by releasing ANP
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9
Q

Where are chemoreceptors? what do they respond to?

A
  • in carotid bodies and aortic arch

- respond to changes in O2 levels

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10
Q

What is function of mechanoreceptors in kidney afferent arterioles?

A
  • activate RAAS
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11
Q

In what conditions do baroreceptors send impulses to medulla?

A
  • more impulses at higher pressure, fewer impulses at decreased pressure
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12
Q

3 phases of baroreceptor response?

A
  1. change in MAP, this is direct response before any reflexes engaged
  2. reflex response tries to change MAP to normal
  3. after changes by reflex, new steady state is reached
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13
Q

pathway of response to acute decreased MAP [ex in hemorrhage]

A
  1. decreased blood volume –> decreased preload –> decreased stroke volume –> decreased CO –> decreased MAP
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14
Q

What happens to SV at higher LVEDP [left ventricular end diastolic pressure]?

A
  • higher LVEDP = more fill, get more ejection of fluid but also a higher percentage of fluid ejected / higher contraction
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15
Q

Do you get more impulses from baroreceptors to medulla at increased or decreased pressure?

A

at increased pressure

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16
Q

What are effects of reduced baroreceptor firing?

A
  • increase S to SA –> increase HR
  • decreased PS to SA –> increase HR
  • increased S to ventricles –> increase contractility
  • increased S to arterioles –> increased TPR
  • increased S to veins –> venoconstriction
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17
Q

What are the 2 molecular mechanisms of the reflex response on HR to low MAP?

A
  1. decreased PS –> decreased activation of IkAch by By subunits
  2. increased S –> increased activation funny current by cAMP
18
Q

What 4 drugs mimic effect of baroreceptor reflex to low MAP [on HR]? What do they do to HR?

A

Atropine: inhibits PS
Isoproterenol: B agonist
Norep/Epi

increase HR

19
Q

What is effect on contractility of reflex response to MAP?

A

increased sympathetic output to ventricles –> increased cellular contractility –> higher SV for same ventricular filling

  • more B stimulation, more camp, more PKA –> phosphorylation L-type Ca channels and phospholamban
20
Q

What 3 drugs mimic effect of baroreceptor reflex on low MAP [on contractility]? What do they do?

A
  • NE, epi, isoproterenol

- increase contractility, faster relaxation, bigger stroke volume

21
Q

What is reflex response on TPR in low MAP? Mech/path?

A
  • more sympathetic output to arteriole smooth muscle cells –> more TPR
  • get more a1 stimulation –> release of Gq a subunit –> activates phospholipase C –> produces IP3 –> SR Ca release [slow compared to RyRs] –> contraction
  • smooth muscle contraction –> increased vessel resistance due to contraction [smaller radius]
22
Q

Drugs that mimic reflex response on TPR in low MAP?

A

acts via a1
NE
phenylephrine [a1 agonist]

23
Q

Drugs that inhibit reflex response on TPR in low MAP?

A

phentolamine [a1 blocker]

24
Q

What is reflex response on venoconstriction in low MAP? what effect does this have?

A
  • increased sympathetic output to veins causes venoconstriction [via a adrenergic stimulation]
  • -> causes reduced venous compliance –> fluid can’t stay stored in veins so goes back to heart –> get increased ventricular filling / preload
25
Q

2 effects of baroreceptor reflex [in low MAP] on myocardium?

A
  • increased HR [SA] –> increases CO

- increased contractility [ventricle] –> increases CO

26
Q

2 effects of baroreceptor reflex [in low MAP] on vessels?

A
  • arteriolar smooth muscle contraction –> increases TPR

- venous smooth muscle contraction –> increases preload –> increases CO

27
Q

Do changes in contractility affect systolic or diastolic?

A

systolic

28
Q

Do changes in arterial pressure affect systolic or diastolic?

A

diastolic

29
Q

When are atrial stretch receptors activated? What do they do?

A

in high blood volume they cause atria to release ANP into bloodstream

30
Q

What does ANP do [2 things]?

A
  • vasodilate blood vessels –> lower TPR –> lower MAP

- block renal Na reabsorption –> increase Na excretion –> lower blood volume

31
Q

In what circumstance does the heart act as an endocrine organ?

A

when atrial stretch receptors activated and release ANP into bloodstream

32
Q

What is function of central chemoreceptors?

A
  • in carotid bodies and aorta
  • response to decrease in blood O2
  • cause vasoconstriction and changes in breathing
33
Q

What is effect of chemoreceptors on vessels?

A
  • low O2 –> chemoreceptors signal to increase S to arterioles –> increased resistance
  • causes vasoconstriction in renal, skeletal muscle, splanchnic [GI] circulations
34
Q

How is blood pressure regulated long term?

A

renin-angiotensin-aldosterone system [RAAS]

35
Q

What is pathway of RAAS?

A
  1. decreased pressure in kidney causes release renin from juxtaglomerular cells
  2. increased renin –> increased angiotensin II
  3. increased angiotensin II which:

——> increased aldosterone –> increased Na reabsorption in kidney –> increased blood volume

——> direct vasoconstriction –> increased TPR

36
Q

Where is renin released from? in response to what?

A
  • released from juxtaglomerular cells in kidney

- in response to decreased pressure in kidney

37
Q

2 steps of angiotensin II release? What enzymes?

A

Renin: activates angiotensinogen –> angiotensin I

angiotensin converting enzyme [ACE]: activates angiotensin I –> angiotensin II

38
Q

What are 2 direct effects of angiotensin II?

A
  1. increases aldosterone

2. vasoconstriction [via increased release of Ca leading to smooth muscle contraction]

39
Q

What is effect of aldosterone?

A

increases Na reabsorption in kidney –> increases blood volume

40
Q

What are 2 effects/pathways induced by angiotensin II?

A

——> increased aldosterone –> increased Na reabsorption in kidney –> increased blood volume

——> activates release of Ca in vascular smooth muscle–> contraction –> vasoconstriction –> increased TPR/BP

41
Q

What is long term effect of angiotensin II?

A
  • Angiotensin II can reset baroreceptor response

- shift curve so have higher HR for a given BP, this keeps BP/MAP up

42
Q

What time fram for baroreceptor vs atrial stretch receptors vs RAAS vs chemoreceptors?

A

baroreceptor reflex = short term change MAP

atrial stretch = medium term change MAP

chemoreceptor = mild change MAP, altered breathing

RAAS = long term change MAP

Physiology Part 1 (37 decks)

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