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Cardiovascular 2018 > Drugs affecting control of blood pressure > Flashcards

Drugs affecting control of blood pressure Flashcards

1
Q

In vascular smooth muscle cell contraction describe how the intracellular concentration of calcium is increased?

A

Through the opening of L-type Ca channel bu numerous depolarizing mechanisms and GPCR receptor coupled to Gq/11

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2
Q

In vascular smooth muscle cell contraction what does intracellular calcium couple to?

A

calmodulin to form Ca-CaM

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3
Q

What role does Ca-CaM play in vascular smooth muscle cell contraction ?

A

It activated Myosin Light Chain Kinase

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4
Q

What does active MLCK do in vascular smooth muscle cell contraction ?

A

It phosphorylates the myosin light chain and causes contraction

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5
Q

What is the role of cGMP in vascular smooth muscle cell relaxation?

A

It activates Protein Kinase G

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6
Q

What is the role of PKG in vascular smooth muscle cell relaxation?

A

Activates myosin-lc phosphatase

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7
Q

What is the role of myosin-lc phosphatase in vascular smooth muscle cell relaxation?

A

It dephosphorylates the myosin light chain, causing relaxation

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8
Q

What do organic nitrates do to VSM?

A

Relax it

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9
Q

What organic nitrates do at clinical doses?

A

Venorelaxation
Increased coronary blood flow
Arteriolar dilatation

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10
Q

What does venorelaxation cause?

A

Reduced preload, then SV but CO is maintained by increased HR

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11
Q

What is the benefit of organic nitrates to patients with angina?

A

Decreased myocardial oxygen requirement

1) decreased preload
2) decreased after load
3) improved perfusion of the ischaemic zone

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12
Q

What is the effect of motivate on the coronary circulation?

A

dilate the collateral vessels, ensuring blood flow to the myocardium is increased

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13
Q

What is the role of endothelin in vascular smooth muscle tone

A

when endothelin is produced as a result of altered gene expression through adrenaline, angiotensin II, ADH or NO, natriuretic peptides or sheer stress it will agonise the Eta receptor, and through numerous signalling pathways including Gw/11 increase intracellular calcium and cause contraction

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14
Q

What is the clinical use of organic nitrates?

A

used in stable and ACS

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15
Q

What are the main organic nitrates used in ACS?

A

GTN and isosorbide mononitrate (occasionally isosorbide dinitrate)

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16
Q

What is the action of GTN?

A

Short acting- excessive first pass metabolism (this is why it is given as a spray or sublingual)

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17
Q

How is GTN given in unstable angina?

A

IV infusion with aspirin to prevent a thrombus

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18
Q

What method can GTN be administered for a long lasting effect?

A

Transdermal patch

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19
Q

What is the action on isosorbide mononitrate like?

A

Longer acting as it is resistant to first pass metabolism

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20
Q

How is isosorbide mononitrate administered?

A

Orally for prophylaxis of angina

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21
Q

What is associated with repeated administration of organic nitrates?

A

Reduced effect- tolerance

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22
Q

Name some unwanted side effects of organic nitrates?

A

Postural hypotension

Headaches

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23
Q

What is the Eta targeted in?

A

Pulmonary hypertension by bosentan and ambrisentan

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24
Q

What causes increased renin release?

A

increased Renal sympathetic nerve activity

decreased Renal perfusion

reduced glomerular filtration

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25
What does the AT1 (GPCR) cause
Increased release of noradrenaline from sympathetic nerves Growth in the heart and arteries as a result of altered gene expression aldosterone release from the adrenal cortex cousin tubular Na reabsorption and salt retention
26
Where is ACE present?
On endothelial cells particularly the cells of the lung
27
Where are AT1 receptors present?
Terminal sympathetic neurons which innervate VSM and VSM cells
28
What do AT1 receptors in the adrenal cortex cause?
synthesis and release of aldosterone which acts to increase salt retention
29
What does ACE do?
Convertes inactive angiotensin I to angiotensin II Inactivates bradykinin (vasodilator)
30
What do ACE inhibitors do?
block the conversion of angiotensin I to angiotensin II
31
What do AT1 receptor antagonists do?
Block the action of angiotensin II at AT1 receptors in a competitive manner
32
What do ACEI do do MABP?
``` Decrease it venous dilatation (decreased preload) and arteriolar dilatation (decreased afterload and decreased TPR) decreasing arterial blood pressure and cardiac load ```
33
What affect do ACEI have on cardiac contractility?
none
34
What do ACEI do to aldosterone release?
Reduce (not abolish) the release of aldosterone (decrease in circulating levels of aldosterone promotes loss of Na+ and H2O)
35
Where do they have the greatest effect and on whom?
much larger effect in hypertensive patients (especially if renin secretion is enhanced – e.g. as a consequence of diuretic therapy) angiotensin-sensitive vascular beds (brain, heart, kidney)
36
What is the additional effect of angiotensin II on the heart and vasculature?
Causes growth
37
What are the adverse effects of ACEI?
hypotension | dry cough
38
What is an essential difference between ARBs and ACEi?
ARBs do not inhibit the metabolism of bradykinin
39
When are ACEI and ARBs contraindicated?
Pregnancy | bilateral renal artery stenosis
40
What are the clinical uses of ARBs and ACEi?
hypertension cardiac failure post MI
41
What is the mechanism by which ACEi and ARBs are used in the treatment of hypertension?
benefit derives from 1) reduced TPR and MABP 2) possible suppression of proliferation of smooth muscle cells in the media of resistance vessels
42
What is the mechanism by which ACEi and ARBs are used in the treatment of cardiac failure?
is associated with inappropriate activation of the RAAS. ACEIs 1) decrease vascular resistance improving perfusion 2) increase excretion of Na+ and H20 3) cause regression of left ventricular hypertrophy
43
What is the function of alpha1 adrenoreceptors?
constrict
44
What is the function of B1 adrenoreceptors?
increase HR increase force of contraction increase AV node conduction velocity
45
What is the role of B2 adrenoreceptors?
bronchorelaxation | vasodilatation
46
Why are B blockers useful in the treatment of angina pectoris?
decrease myocardial O2 requirement (decreased HR & decreased SV = decreased work = decreased O2) counter elevated sympathetic activity associated with ischaemic pain increase the amount of time spent in diastole (decreased HR), improving perfusion of the left ventricle
47
Why are B blockers useful in the treatment of hypertension?
No longer first line BUT reducing cardiac output (MABP = CO x TPR) (However, CO returns to normal over time but MABP remains depressed by ‘resetting’ of TPR at a lower level – mechanism uncertain) reducing renin release from the kidney a CNS action that reduces sympathetic activity
48
Why are B blockers useful in the treatment of heart failure?
In combination with other drugs to suppress adverse effects associated with elevated activity of the sympathetic nervous system and RAAS (Start low, go slow)
49
What do calcium antagonists do?
prevent the opening of L-type channels in excitable tissues in response to depolarization and hence limit intracellular calcium
50
What are L type channels responsible for?
upstroke in the AP in the SA and AV nodes- Ca2+ antagonists can reduce rate and conduction through the AVN phase 2 of the ventricular AP- Ca2+ antagonists can reduce the force of contraction
51
How do a1 adrenoreceptors function in VSM cells?
a1-adrenoreceptors couple to Gq/11 and open the cation selective channels (Na channel) which allows calcium entry into the cell
52
what are the three main types of calcium antagonists?
"verapamil: selective for cardiac L-type channels o physically blocks the L-type channel amlodipine: selective for L-type channels in VSM diltiazem: intermediate selectivity from cardiac and VSM cells o act allosterically
53
What are the clinical uses of calcium antagonists?
Hypertension angina dysrythmias
54
What is the mechanism whereby calcium antagonists work in hypertension?
reduced Ca entry= arteriolar dilatation= reduce TPR & MABP
55
What is the mechanism whereby calcium antagonists work in angina?
prophylactic treatment used with GTN (particularly if B blockers are contraindicated) peripheral arteriolar dilatation- decreasing afterload and myocardial oxygen requirement coronary vasodilatation amlodipine: little effect on cardiac muscle diltiazem and verapamil: negative inotropic effects. some of reduction in cardiac force is compensated by sympathetic system
56
What is the mechanism whereby calcium antagonists work in dysrythmias?
Ventricular rate in rapid atrial fibrillation reduced by suppression of conduction through the AV node Verapamil is usually used, but avoid in heart failure, particularly in combination with a b-block
57
How do potassium channel openers function?
ATP closes the ATP type potassium channels, potassium channel openers have the opposite effect (opens K-ATP channels in VSM- causing the cell to hyperpolarise, moves membrane potential away from threshold- supressing the opening of voltage activated calcium channels- causing relaxation)
58
What is minoxidil used for?
last resort in severe hypertension (causes reflex tachycardia- can be prevented by administration of a B-blocker) causes salt and water retention (alleviated by a diuretic). restores hair in balding men when applied topically.
59
What is nicorandil used for?
opens ATP type potassium channels
60
How do a-1 adrenoreceptor antagonists work?
Cause vasodilatation by blocking vascular a1-adrenoceptors. Reduced sympathetic transmission results in decreased MABP
61
What are the most commonly used a-1 adrenoreceptor antagonists?
prazosin and doxazosin - both are competitive antagonists
62
When do a-1 adrenoreceptor antagonists get moved up the prescribing list?
when patient is suffering from benign prostatic hyperplasia, this is because the muscle tone in the prostate is in part modified by -1 adrenoreceptor and noradrenaline and therefore blockers may relieve some of the effects
63
Adverse effect of a-1 adrenoreceptor antagonists?
postural hypotension

Cardiovascular 2018 (39 decks)

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