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Cardiovascular > Pharmacology- Blood Pressure > Flashcards

Pharmacology- Blood Pressure Flashcards

1
Q

what cause contraction of vascular smooth muscle

A

increase of intercellular calcium done by either l type channels or through the release of calcium from the SR by the activation of Gg/11 proteins

and

myosin light chain kinase

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2
Q

what is responsible for the relaxation of vascular smooth muscle

A

myosin light chain phosphatase

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3
Q

what does Nitric oxide cause when arriving at vascular smooth muscle and how

A

relaxation

by activating calcium activated K channels which removes k from cell hyperpolarisaing it taking it away from threshold and causing relaxation

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4
Q

what mechanisms do organic nitrate drugs activate and how

A

relaxation mechanisms by donating NO which diffuse to smooth muscle cells

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5
Q

what types of muscle do organic nitrates relax

A

all smooth muscle types

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6
Q

what do organic nitrates do to the vasculature

A

venorelaxation (small doses), arteriolar dilatation (higher doses), increased coronary blood flow

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7
Q

what are the effects of venorelaxation

A

decreases pressure in right atrium (CVP) (preload)

reduces SV

CO maintained by increased HR

no change in arterial blood pressure

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8
Q

what are the effects of arteriolar dilatation

A

decreases arteriolar pressure reducing afterload

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9
Q

why are organic nitrates good at treating angina

A

TREATS PAIN ONLY NOT CAUSE

as blood is redirected towards the ischaemic zone

-decreases myocardial oxygen requirement (via decreased preload, afterload and increased perfusion of the ischaemic zone

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10
Q

what are organic nitrates used to treat

A

stable angina and acute coronary syndrome

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11
Q

give three examples of organic nitrates

A

glyceryltrinitrate (GTN)

isosorbide mononitrate (ISMN)

isosorbide dinitrate

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12
Q

what is first pass metabolism

A

when oral drug goes through the liver before getting into systemic system

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13
Q

what are the side effects of organic nitrates

A

tolerance, postural hypotension, headaches

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14
Q

what is endothelin 1 and its receptor

A

potent vasoconstrictors

ETA receptors

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15
Q

what leads to the expression of endothelin 1

A

decreased nitric oxide, shear stress and natriuretic peptides (hormones from chambers of heart)

increased adrenaline, angiotensin II and ADH

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16
Q

what are antagonists of the ETA receptor used in

A

the treatment of pulmonary hypotension

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17
Q

what does the renin-angiotensin-aldosterone system play a major role in the regulation of

A

sodium secretion and vascular tone

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18
Q

what two types of drugs act on the renin-angiotensin-aldosterone system

A

ACE inhibitors and angiotensin receptor antagonists

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19
Q

what three factors lead to increased renin release

A

decrease renal perfusion pressure

increase symp activity

decreased glomerular function

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20
Q

what is contraction of vascular smooth muscles the result of (2)

A

Activation of smooth muscle AT1 receptors

Increased release of noradrenaline from sympathetic nerves

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21
Q

what does renin turn into

A

angiotensin I

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22
Q

what is the receptor for angiotensin II

A

AT1 receptor (GPCR)

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23
Q

what does the contraction of vascular smooth muscle do to mean arterial blood pressure

A

increases it

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24
Q

what part of renin process leads to increased blood volume and MABP

A

aldosterone secretion from adrenal cortex leads to tubular Na+ reasbsorption and salt retention

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25
Q

what is an ARB

A

agiotensin 1 (AT1) receptor blocker

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26
Q

what two types of drugs stop the renin cycle

A

agiotensin converting enzyme inhibitors (ACE inhibitors)

angiotensin 1 (AT1) receptor blockers (ARBs)

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27
Q

what does ACE inhibit

A

bradykinin (vasodilator)

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28
Q

name an ACE inhibitor and what they ALL have in common

A

lisinopril (opril)

29
Q

give an example of a ARB and what they all have in common

A

losartan (sartan at end of name)

30
Q

what do ACE inhibitors cause

A

vasodilatation (decreased preload), arterial dilatation (decreased afterload and TPR)

31
Q

what affect do ace inhibitors have on cardiac contractility

A

none (CO may decrease as a result of decreased TPR)

32
Q

what do ACE inhibitors reduce the release of

A

aldosterone (decrease in Na+ ans H20)

33
Q

what are the side affects of ACE inhibitors

A

hypotension and dry cough

34
Q

do ARBs affect the metabolism of bradykinin

A

no

35
Q

when would you switch from an ACE inhibitor to an ARG

A

to get rid of dry cough

36
Q

what can ACE inhibitors and RGB not be used in

A

pregnancy and bilateral renal artery stenosis

37
Q

what are the clincal uses of ACE inhibitors and AT1 receptor agonists

A

hypertension

cardiac failure

following myocardial infarction

38
Q

what are adrenoceptors

A

G-protein-coupled receptors (GPCRs) that are activated by the sympathetic transmitter noradrenaline (norepinephrine) and the hormone adrenaline (epinephrine)

39
Q

what does the activation of alpha 1 adrenoceptor lead to

A

constriction of vasculature

40
Q

what does activation of Beta 1 adrenoceptor lead to

A

increase heart rate, force, av conduction

41
Q

what does the activation of beta 2 adrenoceptors lead to

A

relax of airway smooth muscle and vascular SM

42
Q

what are the clinical uses of beta adrenoceptor agonists

A

treatment of angina pectoris, hypertension, heart failure

43
Q

what do beta 1 selective agents do

A

decrease myocardial O2 requirement (descrease HR and SV), counter elevated sympathetic activity, increase amount of time spent in diastole (improving perfusion) of the left ventricle)

44
Q

what must happen in order for blood to perfuse the myocardium

A

aortic pressure must exceed ventricle pressure

45
Q

how do beta blocker treat hypertension

A

reduce cardiac output (and therefore MABP), reduce renin release from the kidneys, CNS action that reduces sympathetic activity

46
Q

how do beta blockers reduce renin release from the kidneys

A

renal adrenoceptors

47
Q

what is RAAS

A

renin–angiotensin–aldosterone system

48
Q

how are beta blockers administered when used to treat failure

A

in combination with other drugs to suppress adverse effects associated with elevated activity of the symp system and RAAS

49
Q

what do calcium antagonists do

A

prevent the opening of L-type channels in excitable tissues in response to depolarisation

50
Q

what parts of the AP in SA and AV nodes do the L channels mediate

A

the upstroke, Ca2+ antagonist can reduce rate and conduction through the AV node

51
Q

what parts of the AP in ventricles do the L channels mediate

A

phase 2 (plateau phase), Ca2+ antagonists can reduce force of contraction

52
Q

what is the role of L type channels in vascular smooth muscles

A

provide pathway for entry of Ca2+

53
Q

what are the three main types of calcium antagonist

A

verapamil, amlodipine, diltiazem

54
Q

what is opening of L-type channels caused by

A

activation of a G protein on membrane cells (adrenoceptors coupled to G proteins)

55
Q

how do calcium antagonists treat hypertension

A

reduced Ca2+ entry in to vascular smooth muscles causing arteriolar dilatation (reducing TPR and MABP)

cause coronary dilatiation (treats hypertension and angina)

56
Q

what are the adverse effects of calcium antagonists

A

excessive vasodilatation= hypotension, dizziness, swollen oedema

57
Q

name three calcium antagonists

A

amlodipine, diltiazem and verapamil

58
Q

how can calcium antagonists treat dysrhythmias

A

suppress conduction through the AV node

59
Q

what do potassium channel opener drugs do

A

Open ATP-modulated K+ channels (KATP) channels in vascular smooth muscle

cause hyperpolarisation which switches of L type channels

acts primarily on arterial smooth muscle

60
Q

give two example of potassium channel openers

A

minoxidil and nicorandil

61
Q

what do alpha 1 adrenoceptor receptor agonist

A

cause vasodilatation by blocking vascular alpha 1 adrenoceptor

62
Q

name 2 alpha 1 adrenoceptor antagonists

A

prazosin and doxazosin

63
Q

how does reduced sympathetic output affect MABP

A

decreases it

64
Q

what is the main adverse effect of a1 adrenoceptor receptor antagonists

A

postural hypotension

65
Q

what do diruetics do

A

act on kidney to increase the excretion of Na, Cl and H2O and excert indirect relaxant effects on the vasculature

66
Q

what are the two main types of diuretics

A

thiazides and loop diuretics

67
Q

what is the undesirable effect cause by both types of diuretics

A

loss of K+ (corrected by co-administration of K sparring diuretic/ K+ supplements

68
Q

how can diuretics help in cardiovascular disease

A

dilate vasculature so help in mild heart failure, hypertension, oedema, heart failure

Cardiovascular (34 decks)

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