Direct vasodilators minoxidil

Direct Vasodilators Isosorbide dinitrate 20 mg and hydralazine 37.5 (BiDil) 1-2 tablets three times a day Minoxidil (Loniten) Hydralazine Heart failure (isosorbide dinitrate + hydralazine in African-Americans) A-HeFT66 Edema (minoxidil) Tachycardia Lupus-like syndrome (hydralazine) ... 

Hydralazine and minoxidil cause direct arteriolar smooth muscle relaxation. Compensatory activation of baroreceptor reflexes results in increased sympathetic outflow from the vasomotor center, producing an increase in heart rate, cardiac output, and renin release. Consequently, the hypotensive effectiveness of direct vasodilators diminishes over time unless the patient is also taking a sympathetic inhibitor and a diuretic. 

Pharmacology Minoxidil is a direct-acting peripheral vasodilator. Minoxidil elicits a reduction of peripheral arteriolar resistance. The exact mechanism of action on the vascular smooth muscle is unknown. 

Direct vasodilators frequently produce baroreflex-induced tachycardia, but rarely orthostatic hypotension. They are usually prescribed with a beta blocker or a centrally acting antihypertensive to minimize the reflex increase in heart rate and cardiac output. It should be noted that another member of the directly acting class of antihypertensives is minoxidil. This potent, long-acting drug has gained considerable notoriety for its use as a topical hair-restorer. Oral use can result in hirsutism (unwanted hair growth over the face as well as other parts of the body). 

Minoxidil acts as a direct vasodilator of vascular smooth muscle which decreases peripheral vascular resistance and blood pressure. Veins are affected to a lesser extent than arterioles. The resulting hypotensive effect induces a reflex increase in heart rate, cardiac output, and stroke volume. Sodium and water retention also occur leading to edema plasma renin activity is increased. 

Minoxidil. Minoxidil increases the blood flow to the follicular dermal papilla by a direct vasodilation effect on the arteriolar blood vessels (94, 95). Vasodilation is caused by the active metabolite minoxidil sulfate. 

Direct arterial vasodilators Minoxidil (Loniten) 10 0 1 or 2 Should be used with diuretic and / -blocker to... 

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)... 

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. 

Minoxidil is a peripheral vasodilator that directly relaxes vascular smooth musculature, thus, lowering systolic and diastolic pressure. Its action is linked to the activation of calcium channels. Open calcium channels cause hyperpolarization of smooth muscle cells, which in turn, reduces the flow of calcium ions into the cell, which is necessary for supporting vascular tonicity. However, when taking minoxidil, tachycardia, elevated renin secretion, and water and sodium ion retention all appear simultaneously with hypotension. Because of potentially serious side effects, it is used only for severe hypertension that does not respond to treatment with other drugs, and absolutely in combination with two other antihypertensive drugs. A synonym of this drug is loniten. 

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. 

Correct answer = C. Clonidine reduces sympathetic outflow by stimulating a-adrenergic receptors. Minoxidil is a direct-acting vasodilator. Verapamil causes vasodilation by inhibiting calcium ion flow into smooth muscle. Enalapril blocks the enzyme that converts angiotensin I to angiotensin II. Hydrochlorothiazide acts by decreasing blood volume. 

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

Minoxidil is a direct-acting peripheral vasodilator. The exact mechanism of action on the vascular smooth muscle is unknown. It does not interfere with vasomotor reflexes therefore, it does not prodnce orthostatic hypotension. The drug does not affect CNS fnnction. It appears to block calcium uptake through the cell membrane. Minoxidil reduces elevated systolic and diastolic blood pressnre by decreasing peripheral vascnlar resistance. The blood pressure response to minoxidil is dose-related and proportional to the extent of hypertension. In humans, forearm and renal vascular resistance decline forearm blood flow increases, whereas renal blood flow and GFR are preserved. 

Pinacidil is three- and tenfold more potent than hydralazine and minoxidil, respectively. It does not interact with alpha, beta, cholinergic, or histaminergic receptors, and also does not produce vasodilation via an indirect effect that is mediated by adenosine, prostaglandin, or endothelial-derived relaxant factor. Its vasodilating activity does not resemble that brought about by the conventional calcium-channel antagonists. Thus, pinacidil-induced vascular relaxation is a direct effect mediated by a novel mechanism. 

Drugs that dilate blood vessels by acting directly on smooth muscle cells through nonautonomic mechanisms are useful in treating many hypertensive patients. Three major mechanisms are utilized by vasodilators release of nitric oxide, opening of potassium channels (which leads to hyperpolarization), and blockade of calcium channels (Table 11-3). Compensatory responses are marked for some vasodilators (especially hydralazine and minoxidil) and include salt retention and tachycardia (Table 11-2). 

Nevertheless, it is assumed that treatment with minoxidil lengthens and thickens the small vellus hairs and decreases shedding. Minoxidil is a potassium channel opener that causes vasorelaxation [132] and stimulates cutaneous blood flow to the scalp [133]. Minoxidil sulfate, a metabolite of minoxidil, is a potent vasodilator. Uptake and conversion of minoxidil to minoxidil sulfate occurs within the HE, suggesting a direct action on the follicle [134]. The most probable site of action of minoxidil is the DP [135], and the mechanism of action has been linked to its effects on the Kir6.1/SUR2B potassium channel expressed by the derma papilla [136-138]. 

Minoxidil is a pyrimidine derivative with strong vasodilator properties the action probably results from a direct effect upon the arteriolar smooth muscle and a reduction of the total peripheral vascular resistance. After oral administration maximal blood levels are seen in about one hour, the half-life being about 4.2 hours (ISS ). A hypotensive action is seen later and sometimes only after repeated doses (126 ). 

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