Antihypertensives hemodynamic effects

Because of their capability of lowering the blood pressure regardless of body position, of their overall excellent acceptance by the patients and because of their favorable hemodynamic effects, the diuretic agents remain the most important contribution to antihypertensive therapy. 

In general, the introduction of antihypertensive agents acting on the vasomotor center in the brain appears to be a major advance in the treatment of hypertension. The well balanced hemodynamic effect is far superior to what is observed with inhibition of sympathetic transmission at peripheral sites. Orthostatic hypotension is no longer a problem. It is predicted that pharmacologic progress in this line of compounds will make further contributions to our antihypertensive armamentarium. 

The hemodynamic effects of diazoxide are similar to those of hydralazine and minoxidil. It produces direct relaxation of arteriolar smooth muscle with little effect on capacitance beds. Since it does not impair cardiovascular reflexes, orthostasis is not a problem. Its administration is, however, associated with a reflex increase in cardiac output that partially counters its antihypertensive effects. Propranolol and other -blockers potentiate the vasodilating properties of the drug. Diazoxide has no direct action on the heart. Although renal blood flow and glomerular filtration may fall transiently, they generally return to predrug levels within an hour. 

Moser M. Do different hemodynamic effects of antihypertensive drugs translate into different safety profiles Eur J Chn Pharmacol 1990 38(Suppl 2) S134-8. 

Renal insufficiency is a late complication of hypertension (354). This is why the choice of the antihypertensive drug selected as the firs (dine treatment of a condition that will persist for many years is so important. From this viewpoint, the fall in blood pressure induced by ACE inhibitors might have beneficial renal effects, in addition to those induced by any decrease in perfusion pressure of the kidneys, especially in diabetic patients (222, 355-358). It is unknown if, independendy of the hemodynamic effect, at an early stage of hypertension and before the initiation of a progressive decrease in renal function, a local decrease in angiotensin II (or increase in bradykinin) explains or direcdy participates in a so-called renoprotective effect (359). 

Hemodynamic Effects of Long-Term Administration of Antihypertensive Agents ... 

The vasodilators decrease total peripheral resistance and thus correct the hemodynamic abnormality that is responsible for the elevated blood pressure in primary hypertension. In addition, because they act directly on vascular smooth muscle, the vasodilators are effective in lowering blood pressure, regardless of the etiology of the hypertension. Unlike many other antihypertensive agents, the vasodilators do not inhibit the activity of the sympathetic nervous system therefore, orthostatic hypotension and impotence are not problems. Additionally, most vasodilators relax arterial smooth muscle to a greater extent than venous smooth muscle, thereby further minimizing postural hypotension. 

From a hemodynamic viewpoint, there are several obvious advantages to using a p-blocker in combination with a vasodilator. Rehex-mediated cardiac shmulation is a common feature of vasodilator treatment and can severely hmit its antihypertensive effectiveness. A p-blocker will reduce the cardiac stimulahon and thus preserve the effectiveness of the vasodilator. Conversely, the vasodilator will prevent the increase in peripheral vascular resistance that occurs on initiation of treatment with a p-blocker. Furthermore, vasodilator treatment initiates rehexes that lead to an increase in plasma renin... 

Antihypertensive Agent Mechanism of Action Effects on Renal Hemodynamics... 

Miyagishi et at. Arch. Int. Phamtacodyn. Ther, 271, 249 (1984). Possible anti-anginal effects M. Sakanashi et at, 0yo Yakuri 28, 709 (1984) C.A. 102, 39669z (1985). Long-tcrm antihypertensive effect in rats K. Kishi et at, J. Phar-macobiodyn. 8, 50 (1985). Comparison with timolol, 4.V., nf effect on intraocular pressure and hemodynamics M. 

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