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AntihypertensiveII
lecture 23b mumby
| Question | Answer |
|---|---|
| things that cause renin release | low arterial blood pressure --> activates renal sympathetic tone and intrarenal baroreceptors that sense low afferent arteriole pressures; low Na delivery to macula densa cells also causes renin release |
| effects of angiotensin II (thus benefits of ACE inhibitors are due to dec in these effects) | causes rapid pressor response via catecholamine release from adrenal medulla, causes slower pressor response via release of aldosterone and altered renal hemodynamics, also causes vascular and cardiac hypertrophy and remodeling |
| mechanism/pharm effect of ACE inhibitors | bind ACE and stops creation of AII, lowers BP by reducing peripheral vascular resistance. also happens to stop ACE's inactivation of bradykinin = cough |
| adverse effects of ACEI | cough is the most predominant, angioedema, hypotension due to high levels of renin, hyperkalemia (blocks aldosterone production), can worsen condition of pts with RAS b/c kidney needs AII to maintain GFR, fetopathic |
| angiotensin receptor antagonists | Losartan: competitive antagonists of type I AIIR in vascular smooth muscle. adverse effects are hyperkalemia and hypotension. protective effects in pts with LVH, renal-protective |
| renin inhibitor | Aliskiren: high affinity competitive inhibitor of renin, reduces conc'ns 50-80% and effectively lowers both SBP and DBP |
| benefits of using ACEI for HTN tx | besides obvi reasons they slow diabetic glomerulonephropathy, chronic renal dz, decrease morbidity of pts with CHF or post-MI, protective in pts with CV dz |
| Ca channel blockers | DHP class: nifedipine and non-DHP class: verapamil and diltiazem. all kinds inhibit Ca influx into arterial smooth muscle, causing a decrease in resistance after relaxation occurs, may cause a mild sympathetic response |
| effects that diltiazem and verapamil have that nifedipine would not | non-DHP CCBs actually cause a modest dec in HR by inhibiting Ca channels in SA and AV nodes in addition to dec arterial PVR. no real change in contractility due to dec afterload and dec chronotropy even with reflex inc in adrenergic tone |
| relative potency of arterial vasodilation among CCBs | nifedipine (notorious for causing horrible reflex tachy if d/c quickly) >> verapamil > diltiazem |
| therapeutic uses of CCBs | tx of HTN by relaxing arteriolar smooth muscle and dec PVR. good for low-renin HTN, don't really cause fluid retention like some other antihypertensives. BUT don't use in pts with SA or AV node dysfunction or CHF |
| metoprolol pharm effect | initially dec CO with reflex inc in PVR, but after hrs to days PVR returns to nl with sustained dec CO = lowered BP |
| direct arteriolar vasodilators | hydralazine and monoxidil act directly on smooth muscle of arterioles to vasodilate, almost always used as second or third line drugs for very hypertensive pts refractory to other tx options |
| hydralazine | direct vasodilator, works very potently. can cause H/A, nausea, flushing, hypotension, palpitations, tachy, dizziness all due to potent central vasodilation. |
| minoxidil | activates ATP-sensitive K channels in vascular smooth muscle and causes hyperpolarization. very powerful arterial vasodilator and stimulator of renin secretion. causes fluid and salt retention, caution strong symp reflex & hypertrichosis |
| sodium nitroprusside | vasodilator used in hypertensive emergencies; works on cGMP-dependent kinase to cause dec in intracellular Ca and relaxation of veins and arteries. causes only a modest increase in HR and oxygen demand |
Created by:
sirprakes
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