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Minoxidil Hydralazine

The answer is d. (Hardman, pp 794-795.) Hydralazine, minoxidil, diazoxide, and sodium nitroprusside are all directly acting vasodilators used to treat hypertension. Because hydralazine, minoxidil, nifedipine, and diazoxide relax arteriolar smooth muscle more than smooth muscle in venules, the effect on venous capacitance is negligible. Sodium nitroprusside, which affects both arterioles and venules, does not increase cardiac output, a feature that enhances the utility of sodium nitroprusside in the management of hypertensive crisis associated with MI. [Pg.126]

In contrast to hydralazine, minoxidil, and diazoxide, sodium nitroprusside relaxes venules as well as arterioles. Thus, it decreases both peripheral vascular resistance and venous return to the heart. This action limits the increase in cardiac output that normally follows vasodilator therapy. Sodium nitroprusside does not inhibit sympathetic reflexes, so heart rate may increase following its administration even though cardiac output is not... [Pg.230]

Minoxidil is a very efficacious orally active vasodilator. The effect results from the opening of potassium channels in smooth muscle membranes by minoxidil sulfate, the active metabolite. Increased potassium permeability stabilizes the membrane at its resting potential and makes contraction less likely. Like hydralazine, minoxidil dilates arterioles but not veins. Because of its greater potential antihypertensive effect, minoxidil should replace hydralazine when maximal doses of the latter are not effective or in patients with renal failure and severe hypertension, who do not respond well to hydralazine. [Pg.235]

The release of renin is altered by a wide variety of pharmacologic agents. Renin release is stimulated by vasodilators (hydralazine, minoxidil, nitroprusside), 13-adrenoceptor agonists, cx-adrenoceptor antagonists, phosphodiesterase inhibitors (eg, theophylline, milrinone, rolipram), and most diuretics and anesthetics. This stimulation can be accounted for by the control mechanisms just described. Drugs that inhibit renin release are discussed below. [Pg.376]

VASODILATOR ANTIHYPERTENSIVES BETA-BLOCKERS t hypotensive effect Additive hypotensive effect with diazoxide, hydralazine, minoxidil and sodium nitroprusside. In addition, hydralazine may T the bioavailability of beta-blockers with a high first-pass metabolism (e.g. propanolol and metoprolol), possibly due to alterations in hepatic blood flow or inhibited hepatic metabolism Monitor BP closely... [Pg.47]

NITRATES ANALGESICS-NSAIDS Hypotensive effects of hydralazine, minoxidil and nitroprusside antagonized by NSAIDs NSAIDs cause sodium and water retention in the kidney and can raise BP due to 1 production of vasodilating renal prostaglandins Monitor BP at least weekly until stable... [Pg.132]

Direct vasodilator agents T Renal vascular resistance (hydralazine, minoxidil) Arterial vasodilation plus dilatation of venous capacitance vessels (nitroprusside) Increase in RBF and no effect on GFR Decrease in GFR and RBF (acute effect)... [Pg.809]

Direct-acting vasodilators lower the peripheral vascular resistance mainly by causing arteriolar dilation. Drugs discussed are nitroprusside, hydralazine, minoxidil, and diazoxide. [Pg.103]

However, the probable best usage of propranolol shall be its combination with an antihypertensive vasodilators e.g. hydralazine, minoxidil etc., to preferentially check and prevent the reflex tachycardia. ... [Pg.396]


See other pages where Minoxidil Hydralazine is mentioned: [Pg.46]    [Pg.46]    [Pg.546]    [Pg.300]    [Pg.39]    [Pg.98]    [Pg.545]    [Pg.1139]   
See also in sourсe #XX -- [ Pg.899 ]




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