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PMCOL 200 > Lecture 27 - High Blood Pressure > Flashcards

Lecture 27 - High Blood Pressure Flashcards

1
Q

the force of blood against artery walls as it circulates through the body (essential for distributing blood throughout the body)

A

blood pressure

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2
Q

true or false: blood pressure changes throughout the cardiac cycle

A

true

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3
Q

the maximum blood pressure during contraction of the ventricles

A

systolic pressure

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4
Q

the minimum pressure recorded just prior to the next contraction (ventricular relaxation)

A

diastolic pressure

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5
Q

one of the main risk factors for heart disease (contributes to nearly 10.8 million deaths every year), as well as cerebrovascular and renal disease

A

hypertension

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6
Q

does the incidence of high blood pressure increase with age?

A

yes

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7
Q
  • high sodium intake
  • low potassium
  • overweight/obesity
  • unhealthy diet
  • cigarette smoking
  • alcohol consumption
  • sedentarism
  • stress
  • sleep disorders
    these are all examples of:
A

modifiable risk factors of hypertension

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8
Q
  • age
  • existing health
  • conditions
  • ethnicity
  • family history
    these are all examples of:
A

non-modifiable risk factors of hypertension

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9
Q

blood presure is primarily regulated by the _____ through their influence on _____

A

sympathetic nevours system and kidneys, cardiac output and peripheral vascular resistance

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10
Q

what is the formula for blood pressure?

A

BP = cardiac output (CO) x peripheral vascular resistance (PVR)

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11
Q

the amount of blood pumped out by each ventricle per minute

A

cardiac output (CO)

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12
Q

the resistance in the circulatory system that is used to create blood pressure

A

peripheral vascular resistance (PVR)

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13
Q

what are the three critical sites/mechanisms were drugs regulate blood pressure?

A
  • the heart
  • resistance vessels
  • renin-angiotensin-aldosterone system (RAAS)
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14
Q

a complex multi-organ endocrine system invovling the kidneys, adrenal glands, and vasculature

A

the renin-angiotensin-aldosterone system (RAAS)

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15
Q

drugs that control how hard the heart is pumping

A

beta-blockers and diuretics

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16
Q

drugs that control what the heart is pumping against

A

alpha-blockers (not commonly used to treat blood pressure)

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17
Q

go review slide 822

A

nephrons wooooo

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18
Q

drugs that get rid of excess water in the body

A

diuretics

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19
Q

what do diuretics do?

A

they increase urine production in the kidneys, which lowers the blood pressure in the blood vessels

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20
Q

thiazide diurectics are effective in lowering blood pressure by:

A

10-15mmHg

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21
Q

what is the mechanism of action of thiazide diuretics?

A

inhibition of the Na+/Cl- cotransporter (NCC) in the renal distal convoluted tubule

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22
Q

what is the effect of inhibiting the Na+/Cl- cotransporter (NCC)?

A

decreases sodium reabsorption and increases sodium and water exrection (water follows sodium)

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23
Q

GPCRs which are activated by catecholamines such as adrenaline (epinephrine) and noradrenaline (norepinephrine)

A

adrenergic receptors (ARs)

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24
Q

these receptors are an important target for regulating blood pressure

A

adrenergic receptors (ARs)

25
what are the two major subgroups of adrenergic receptors (ARs)?
alpha and beta-adrenoceptors
26
what is the predominant adrenergic receptor in the heart?
beta-1
27
what is the effect of beta-1 adrenergic receptors on the heart?
responsible for acceleration of the heart rate and causing the heart to pump harder during a 'fight or flight' response
28
what are the steps of beta-1 adrenergic receptor activation?
- activation of adenylate cyclase - production of cAMP - production of PKA - increased expression of voltage gated Ca++ (L-type) channels, ryanodine receptors (RyRs), and SERCA pumps
29
what kind of receptor is the beta-1 adrenergic receptor?
a GPCR (Gs)
30
what are the three major effects of beta-1 adrenergic receptor activation in the cell?
- increase Ca++ influx - increase Ca++ release (from internal stores) - increase Ca++ reuptake
31
responsible for the release of Ca++ from itracellular stores during excitation-contraction
ryanodine receptors (RyRs)
32
transport Ca++ from the cytosol back to the sarcoplasmic reticulum following muscle contraction
SERCA pumps
33
in the lungs and certain blood vessels, ____ are the predominant adrenergic receptors
beta-2 adrenergic receptors
34
what are the effects of activating beta-2 adrenergic receptors?
causes bronchodilation , enhancing blood flow to skeletal muscles during a 'fight or flight' response
35
in vascular and bronchiolar smooth muscle, protein kinase A (PKA) plays a key role in relaxation by:
inhibiting myosin light chain kinase (MLCK)
36
normally promotes smooth muscle cell contraction by phosphorylating myosin light chains
myosin light chain kinase (MLCK)
37
what happens when PKA phosphorylates (aka inhibits) myosin light chain kinase (MLCK)?
prevents contraction and leads to smooth muscle relaxation
38
beta-1 and beta-2 adrenergic receptors are both coupled to:
Gs (same early steps of the cascade, but have different effectors)
39
MLCK activation is enabled by:
intracellular Ca++ binding to calmodulin (MLCK is a Ca++-calmondulin dependent protein kinase)
40
in cardiac muscle (predominate beta-1), the key targets of PKA are:
- L-type voltage gated Ca++ channels - ryanodine receptors (RyR2) - SERCA pumps
41
in vascular/bronchiolar smooth muscle (predominate beta-2), the key targets of PKA are:
- myosin light chain kinase (MLCK)
42
pharmacological agents that block the action of endogenous catecholamines on beta-adrenergic receptors, and are part of the sympathetic nervous system
beta-blockers
43
true or false: beta-blockers are not commonly used to treat hypertension
false, they are a widely used treatment
44
the anti-hypertensive effects of beta-blockers are mediated primarily by:
- a decrease in cardiac output by decreasing the heart rate and contractibility - inhibition of renin secretion
45
are beta-blockers competitive or non-competitive antagonists of adrenergic receptors?
competitive antagonists
46
non-selective beta-blockers can affect both:
beta-1 and beta-2 receptors
47
why is it not recommended for non-selectvie beta-blockers to be used in patients with asthma?
due to potential bronchoconstriction from blocking beta-2
48
true or false: alpha adrenergic receptor antagonists are commonly used to treat high blood pressure
false
49
in tissues that do not require increased blood flow during a fight or flight response, _____ are the primary adrenergic receptors in use
alpha-1
50
alpha-1 receptors are coupled to:
Gq proteins (activate phospholipase C)
51
how do alpha-1 receptors mediate their effects?
via inositol phospholipase (IP3) and diacylglycerol (DAG)
52
activation of alpha-1 receptors causes:
vasoconstriction of arterioles
53
inhibition of alpha-1 receptors causes:
vasodilation of arterioles
54
a drug that has non-specific inhibition of alpha-receptors, which leads to an additional effect in reducing peripheral resistance
carvedilol
55
why are selective alpha-1 blockers used for chronic treatment of primary hypertension and not non-selective alpha-blockers?
they produce less reflex tachycardia
56
go review slide 841
good review of your adrenergic receptors
57
refers to factors that influence cardiac contractility
inotropic
58
refers to factors that influence heart rate
chronotropic

PMCOL 200 (35 decks)

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