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PMCOL 200 > Hypertension > Flashcards

Hypertension Flashcards

(72 cards)

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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
what does phosphorylation of MLCK cause?
smooth muscle to relax (bronchial dilation, vasodilation)
26
how can you remember that B1 receptors are in the heart and B2 are in the lungs?
"1 Heart, 2 Lungs"
27
how does phosphorylation of MLCK cause muscle relaxation?
MLCK phosphorylates MLC for contraction, phosphorylated MLCK has inhibited phosphorylative activity and decr muscle contraction
28
what are B-blockers?
competitive antagonists of adrenergic receptors (similar structure to agonists)
29
what are the 2 anti-hypertensive effects mediated by B-blockers?
decr in CO and inhibition of renin secretion
30
what drugs are given to treat hypertension (high BP)?
B-blockers
31
what does inotropic refer to?
influences cardiac contractility (force)
32
what does chronotropic refer to?
influences heart rate
33
is the main effect of B1 adrenergic receptors inotropic or chronotropic?
inotropic
34
what do non-specific B-blockers cause?
inhibit some a-adrenergic receptors which causes vasodilation
35
what is a harm of B-blockers?
bronchospasm (B2 in bronchial smooth muscle) due to non-specific B-blockers (especially in ppl w asthma or resp issues)
36
where are a-adrenergic receptors primarily?
in tissues that don't require incr blood flow during flight-or-flight (intestine)
37
what does stimulation of a-adrenergic receptors cause?
smooth muscle contraction (vasoconstriction)
38
what does inhibition of a-adrenergic receptors cause?
vasodilation
39
what kind of receptors are a-adrenergic?
Gq GPCR (PLC, PIP2)
40
how does activation of a-adrenergic receptors cause vasoconstriction?
IP3 incr intracellular [Ca], interacts w calmodulin which binds to MLCK and incr phosphorylation of MLC (incr contractile F)
41
what does DAG do in the cell to cause vasoconstriction?
DAG activates PKC which phosphorylates Rho kinase which inhibits MLCP (incr contraction)
42
what does blocking a-adrenergic receptors cause?
vasodilation (decr smooth muscle contraction by decr MLCK and incr MLCP)
43
what is an example of a B1 selective blocker?
atenolol
44
what is an example of a non-selective B1/2 blocker?
propranolol (B2-lungs, can effect ppl w resp conditions)
45
what is an example of a non-specific a/B adrenergic blocker?
carvedilol (decr peripheral R and CO)
46
what are the agonist vs antagonist effects at the a1 receptor?
agonist: vasoconstriction (decr activity) antagonist: vasodilation (incr activity)
47
what are the agonist vs antagonist effects at the B1 receptor?
agonist: incr cardiac contractility and rate antagonist: decr cardiac contractility and rate
48
what are the agonist vs antagonist effects at the B2 receptor?
agonist: relaxation of airways and vascular smooth muscle antagonist: constriction of airways and vascular smooth muscle
49
what are 3 functions of the RAAS system?
regulates blood V, salt balance and BP
50
what does the RAAS system include?
kidneys, adrenal cortex and vasculature
51
what are the 4 key components of the RAAS biochemical pathway?
renin, ACE, AT2, aldosterone
52
what is renin?
enzyme secreted by kidney that converts angiotensinogen to angiotensin 1 (AT1)
53
what is ACE?
angiotensin converting enzyme that converts AT1 to AT2
54
what is AT2?
vasoactive peptide that causes vascular smooth muscle constriction and aldosterone release
55
what is aldosterone?
steroid hormone that promotes Na and H2O reabsorption in kidney (not pre packaged into vesicles)
56
what stimulates release of renin?
B1 receptor activation (eg. NE)
57
what would be the effect of B-blockers on renin secretion?
decr renin secretion (blocks B1 receptor in kidney)
58
how does ACE primarily exist?
membrane bound protein in pulmonary capillary endothelium
59
what receptor mediates effects of AT2?
AT2 receptor (type 1) - can be called AT1 receptor
60
what kind of receptors are AT2 type 1 receptors?
Gq GPCR
61
what are effects of AT2 binding to its receptor in adrenal cortex vs vascular smooth muscle?
AC: IP3 -> Ca release -> triggers release of aldosterone VSM: Ca-CaM -> MLCK -> phos MLC -> vasoconstriction
62
how does aldosterone incr Na and H20 reabsorption in distal convoluted tubule?
incr transcription of Na/Cl cotransporter (NCC), Na/K pump, epi Na channel (ENaC)
63
what 2 drugs mediate the RAAS system?
ACE inhibitors, AT1 blockers (ARBs, AT2 type 1 receptor)
64
what do ACE inhibitors do? ex?
prevents ACE from cleaving AT1 to AT2; captopril
65
what is a common side effect ACE inhibitors? why?
dry cough; bradykinin-mediated bronchoconstriction (on-target)
66
what do AT1 blockers do? ex?
inhibits vasoconstrictive effects of AT2 (vasodilation), decr aldosterone secretion; losartan
67
are ACE inhibitors or ARBs better tolerated? why?
ARBs; act downstream of bradykinin (bypass bronchoconstriction/dry cough effects)
68
what are aldosterone antagonists? ex?
competitive antagonist for aldosterone receptor; spironolactone
69
what are the effects of aldosterone antagonists?
diuretic (incr H2O secretion)
70
is it better or worse to use anti-hypertensive drugs together?
better, has additive effects
71
what is used as a marker for overall health?
BP
72
what type of receptors are B1 adrenergic receptors?
Gs GPCRs

PMCOL 200 (27 decks)

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