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PMCOL 200 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Why is blood P essential?

A

Distributes blood throughout body

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2
Q

How is BP generated?

A

Beating of heart and resistance

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3
Q

When is BP highest & lowest during the cardiac cycle?

A

Highest: Sysolic P
Lowest: Diastolic P

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4
Q

What is a normal BP?

A

120/80

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5
Q

What is a hypertensive BP range?

A

≥ 140/90

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6
Q

What does high BP incr the risk of?

A

adverse cardiovascular outcomes

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7
Q

What is the equation for BP?

A

Cardiac output x peripheral vascular resistance

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8
Q

What 3 sites are targeted by drugs that treat high BP?

A

Heart (CO), resistance vessels, RAAS

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9
Q

What does RAAS stand for?

A

Renin-Angiotensin-Aldosterone system

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10
Q

Which section of the kidney is targeted by thiazide diuretics?

A

The distal convoluted tubule

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11
Q

How do thiazides work?

A

Inhibit NaCl reabsorption by blocking Na/Cl cotransporters (NCC) which decr water reabsorption and blood V (also vasodilator)

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12
Q

What is a commonly used thiazide?

A

Bendroflumethiazide

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13
Q

What kind of receptors are adrenergic receptors?

A

GPCRs

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14
Q

What is the major adrenergic receptor in the heart?

A

B1

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15
Q

in cardiac muscle, what are 3 substrates for PKA?

A
  1. L-type Ca channels (V-gated)
  2. Ryanodine receptors
  3. SERCA pumps
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16
Q

what does activation of B1 adrenergic receptors cause in cardiac muscle cells?

A

incr Ca influx, release (CICR) and reuptake (incr F and decr time of contraction)

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17
Q

what is a major receptor in the lungs and some vasculature (skeletal)?

A

B2 adrenergic receptors

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18
Q

what does activation of B2 adrenergic receptors cause?

A

bronchial dilation, incr perfusion to skeletal muscle

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19
Q

what is similar and different btwn B1 and B2 adrenergic receptors?

A

both Gs but have different effectors/substrates for PKA

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20
Q

what is the major target for PKA in B2 signalling cascades?

A

myosin light chain kinase (MLCK)

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21
Q

what is MLCK?

A

protein that enables contraction of smooth muscles

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22
Q

what do V-gated L-type Ca channels do?

A

incr intracellular [Ca] from extracellular influx during heartbeat

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23
Q

what do ryanodine receptors do?

A

incr [Ca] from intracellular stores during heartbeat

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24
Q

what do SERCA pumps do?

A

reuptake Ca into ER stores at end of heartbeat (phospholamban: PKA target)

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25
Q

what does phosphorylation of MLCK cause?

A

smooth muscle to relax (bronchial dilation, vasodilation)

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26
Q

how can you remember that B1 receptors are in the heart and B2 are in the lungs?

A

“1 Heart, 2 Lungs”

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27
Q

how does phosphorylation of MLCK cause muscle relaxation?

A

MLCK phosphorylates MLC for contraction, phosphorylated MLCK has inhibited phosphorylative activity and decr muscle contraction

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28
Q

what are B-blockers?

A

competitive antagonists of adrenergic receptors (similar structure to agonists)

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29
Q

what are the 2 anti-hypertensive effects mediated by B-blockers?

A

decr in CO and inhibition of renin secretion

30
Q

what drugs are given to treat hypertension (high BP)?

A

B-blockers

31
Q

what does inotropic refer to?

A

influences cardiac contractility (force)

32
Q

what does chronotropic refer to?

A

influences heart rate

33
Q

is the main effect of B1 adrenergic receptors inotropic or chronotropic?

34
Q

what do non-specific B-blockers cause?

A

inhibit some a-adrenergic receptors which causes vasodilation

35
Q

what is a harm of B-blockers?

A

bronchospasm (B2 in bronchial smooth muscle) due to non-specific B-blockers (especially in ppl w asthma or resp issues)

36
Q

where are a-adrenergic receptors primarily?

A

in tissues that don’t require incr blood flow during flight-or-flight (intestine)

37
Q

what does stimulation of a-adrenergic receptors cause?

A

smooth muscle contraction (vasoconstriction)

38
Q

what does inhibition of a-adrenergic receptors cause?

A

vasodilation

39
Q

what kind of receptors are a-adrenergic?

A

Gq GPCR (PLC, PIP2)

40
Q

how does activation of a-adrenergic receptors cause vasoconstriction?

A

IP3 incr intracellular [Ca], interacts w calmodulin which binds to MLCK and incr phosphorylation of MLC (incr contractile F)

41
Q

what does DAG do in the cell to cause vasoconstriction?

A

DAG activates PKC which phosphorylates Rho kinase which inhibits MLCP (incr contraction)

42
Q

what does blocking a-adrenergic receptors cause?

A

vasodilation (decr smooth muscle contraction by decr MLCK and incr MLCP)

43
Q

what is an example of a B1 selective blocker?

44
Q

what is an example of a non-selective B1/2 blocker?

A

propranolol (B2-lungs, can effect ppl w resp conditions)

45
Q

what is an example of a non-specific a/B adrenergic blocker?

A

carvedilol (decr peripheral R and CO)

46
Q

what are the agonist vs antagonist effects at the a1 receptor?

A

agonist: vasoconstriction (decr activity)
antagonist: vasodilation (incr activity)

47
Q

what are the agonist vs antagonist effects at the B1 receptor?

A

agonist: incr cardiac contractility and rate
antagonist: decr cardiac contractility and rate

48
Q

what are the agonist vs antagonist effects at the B2 receptor?

A

agonist: relaxation of airways and vascular smooth muscle
antagonist: constriction of airways and vascular smooth muscle

49
Q

what are 3 functions of the RAAS system?

A

regulates blood V, salt balance and BP

50
Q

what does the RAAS system include?

A

kidneys, adrenal cortex and vasculature

51
Q

what are the 4 key components of the RAAS biochemical pathway?

A

renin, ACE, AT2, aldosterone

52
Q

what is renin?

A

enzyme secreted by kidney that converts angiotensinogen to angiotensin 1 (AT1)

53
Q

what is ACE?

A

angiotensin converting enzyme that converts AT1 to AT2

54
Q

what is AT2?

A

vasoactive peptide that causes vascular smooth muscle constriction and aldosterone release

55
Q

what is aldosterone?

A

steroid hormone that promotes Na and H2O reabsorption in kidney (not pre packaged into vesicles)

56
Q

what stimulates release of renin?

A

B1 receptor activation (eg. NE)

57
Q

what would be the effect of B-blockers on renin secretion?

A

decr renin secretion (blocks B1 receptor in kidney)

58
Q

how does ACE primarily exist?

A

membrane bound protein in pulmonary capillary endothelium

59
Q

what receptor mediates effects of AT2?

A

AT2 receptor (type 1) - can be called AT1 receptor

60
Q

what kind of receptors are AT2 type 1 receptors?

61
Q

what are effects of AT2 binding to its receptor in adrenal cortex vs vascular smooth muscle?

A

AC: IP3 -> Ca release -> triggers release of aldosterone
VSM: Ca-CaM -> MLCK -> phos MLC -> vasoconstriction

62
Q

how does aldosterone incr Na and H20 reabsorption in distal convoluted tubule?

A

incr transcription of Na/Cl cotransporter (NCC), Na/K pump, epi Na channel (ENaC)

63
Q

what 2 drugs mediate the RAAS system?

A

ACE inhibitors, AT1 blockers (ARBs, AT2 type 1 receptor)

64
Q

what do ACE inhibitors do? ex?

A

prevents ACE from cleaving AT1 to AT2; captopril

65
Q

what is a common side effect ACE inhibitors? why?

A

dry cough; bradykinin-mediated bronchoconstriction (on-target)

66
Q

what do AT1 blockers do? ex?

A

inhibits vasoconstrictive effects of AT2 (vasodilation), decr aldosterone secretion; losartan

67
Q

are ACE inhibitors or ARBs better tolerated? why?

A

ARBs; act downstream of bradykinin (bypass bronchoconstriction/dry cough effects)

68
Q

what are aldosterone antagonists? ex?

A

competitive antagonist for aldosterone receptor; spironolactone

69
Q

what are the effects of aldosterone antagonists?

A

diuretic (incr H2O secretion)

70
Q

is it better or worse to use anti-hypertensive drugs together?

A

better, has additive effects

71
Q

what is used as a marker for overall health?

72
Q

what type of receptors are B1 adrenergic receptors?

PMCOL 200 (27 decks)

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