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Hydralazine, blood pressure lowering effect

ANG II is also known to induce release of catecholamines from the adrenal medulla and to suppress the reflex inhibition of the heart rate, with the latter probably the inhibiting vagal (cholinergic) neurons to the heart. This has a specific clinical effect that is useful in the use of ACE inhibitors as antihypertensives (see later) namely, the absence of reflex tachycardia seen with other types of blood pressure-lowering drugs such as a-blockers, diazoxide, hydralazine, and ganglionic blockers. [Pg.452]

The first successful drug treatments for hypertension were introduced after World War II. By that time, researchers had learnt that blocking the sympathetic nervous system could lower blood pressure. In 1946, tetraethyl-ammonium, a drug known for 30 years to block nerve impulses, was introduced as a treatment for hypertension. Hexamethonium, an improved version of tetraethylammo-nium, was available for use by 1951. Another effective blood pressure-lowering drug, hydralazine, resulting from the search for antimalarial compounds, was diverted to the treatment of hypertension when it was found to have no antimalarial activity, but to lower blood pressure and increase kidney blood flow. [Pg.11]

The same inheritance controls the acetylation (deactivation) of the antibacterial sulfonamides, the anti-arrhythmic cardiac drug, procainamide (7.56) (Woosley et aL, 1978), the blood-pressure-lowering drug, hydralazine 11.47), and the amine derived by metabolism of the sedative, nitrazepam (12.98). In each case, rapid acetylation reduces the effect of the drug, but slow acetylators of hydralazine are unfortunate for they are prone to develop systemic lupus erythematosis, with arthritis-like symptoms (Batchelor a/., 1980). [Pg.378]

Pharmacokinetics Hydralazine is rapidly absorbed after oral use. Half-life is 3 to 7 hours. Protein binding is 87%, and bioavailability is 30% to 50%. Plasma levels vary widely among individuals. Peak plasma concentrations occur 1 to 2 hours after ingestion duration of action is 6 to 12 hours. Hypotensive effects are seen 10 to 20 minutes after parenteral use and last 2 to 4 hours. Slow acetylators generally have higher plasma levels of hydralazine and require lower doses to maintain control of blood pressure. Hydralazine undergoes extensive hepatic metabolism it is excreted in the urine as active drug (12% to 14%) and metabolites. [Pg.565]

Most of the effects of hydralazine are confined to the cardiovascular system. The decrease in blood pressure after administration of hydralazine is associated with a selective decrease in vascular resistance in the coronary, cerebral, and renal circulations, with a smaller effect in skin and muscle. Because of preferential dilation of arterioles over veins, postural hypotension is not a common problem hydralazine lowers blood pressure equally in the supine and upright positions. [Pg.326]

Hydralazine (apresoline) causes direct relaxation of arteriolar smooth muscle, possibly secondary to a fall in intracellular Ca concentrations. The drug does not dilate epicardial coronary arteries or relax venous smooth muscle. Hydralazine-induced vasodilation is associated with powerful stimulation of the sympathetic nervous system, likely due to baroreceptor-mediated reflexes, which results in increased heart rate and contractility, increased plasma renin activity, and fluid retention all of these effects counteract the antihypertensive effect of hydralazine. Although most of the sympathetic activity is due to a baroreceptor-mediated reflex, hydralazine may stimulate NE release from sympathetic nerve terminals and augment myocardial contractility directly. Most of hydralazine s effects are confined to the cardiovascular system the decrease in blood pressure after administration is associated with a selective decrease in vascular resistance in the coronary, cerebral, and renal circulations, with a smaller effect in skin and muscle. Because of preferential dilation of arterioles, postural hypotension is not common, and hydralazine lowers blood pressure equally in the supine and upright positions. [Pg.556]

For a few years, hexamethonium and hydralazine were mainstays in the treatment of severe hypertension. They were reasonably effective in lowering blood pressure, but often caused severe side-effects. The final dmg developed in those early days, reserpine, was the product of more than two decades of research into compounds derived from Rauwolfia serpentina, a plant used for centuries by physicians and herbalists on the Indian subcontinent. The quality of the result obtained with the various dmgs used in mono- or combined therapy to treat hypertension proved clearly that fatal outcomes associated with this disease are caused by high blood pressure. ... [Pg.11]

MDL 899 (26) is a direct acting arteriolar vasodilator in man, but coadministration of a beta-blocker is necessary to prevent reflex-related side effects. A clinical study with cadralazlne (ISF 2469, 27) shows this compound similar to hydralazine with fewer side effects. Two other vasodilators, budralazine (28) and pinacidil (29) may owe some of their activity to calcium channel blockade.Anthranilamlde (WIN 48,049) lowers blood pressure in monkeys without accompanying tachycardia. This compound acts primarily as a direct vasodilator but also has sympatholytic and dopaminergic activities. Compounds and 32 also lower blood pres-... [Pg.63]


See other pages where Hydralazine, blood pressure lowering effect is mentioned: [Pg.26]    [Pg.573]    [Pg.168]    [Pg.169]    [Pg.12]    [Pg.12]    [Pg.241]    [Pg.242]    [Pg.255]    [Pg.256]    [Pg.283]    [Pg.169]    [Pg.464]    [Pg.148]    [Pg.66]    [Pg.66]    [Pg.66]    [Pg.104]   
See also in sourсe #XX -- [ Pg.573 ]




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