Minoxidil—an alternative to nephrectomy for refractory hypertension

Pettinger, William A.; Mitchell, Helen C.

doi:10.1097/00003246-197309000-00021

Cited by 25 publications

(36 citation statements)

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“…There was no correlation between antihypertensive effect and plasma apparent hydralazine measured by a nonspecific method. 3 In addition, we have shown that acetylator phenotype is inversely related to hypoten-sive response following oral administration of a standard (1 mg/kg) dose of hydralazine. The mechanism by which the acetylator index determines the response to hydralazine is probably related to its influence on hydralazine bioavailability and thereby on hydralazine plasma concentration."…”

mentioning

confidence: 91%

Plasma concentration and acetylator phenotype determine response to oral hydralazine.

Shepherd¹,

McNay

Ludden

et al. 1981

Hypertension

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SUMMARYThe vasodepressor response to single and multiple oral doses of hydralazine, 1 mg/kg, was studied in hypertensive patients. The concentration of bydralazbe in plasma was measured both by a newly developed specific and a nonspecific assay similar to those used in previous studies. Acetylator phenotype was determined following oral sulfamethazine. Plasma hydralazine concentration peaked at 1 hour after administration and was undetectable 2 hours later. Apparent hydralazine was present in plasma in higher concentration and for a longer duration than hydralazine. The peak decreases in blood pressure (BP) were proportional to plasma hydralazine concentration following administration of both single and multiple doses and were substantially maintained for 8 hours.

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mentioning

confidence: 91%

Plasma concentration and acetylator phenotype determine response to oral hydralazine.

Shepherd¹,

McNay

Ludden

et al. 1981

Hypertension

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“…, , peridinopyrimidine-3-oxide is a long-acting orally anesthesia. The mechanism ofrelaxation ofvascular , " , smooth muscle has been reported to be related to effective hypotensive agent (6,9,27), In rats, dogs, th K+ hannel azoni t rt f . idil I ' , ,.…”

Section: Introduction Histaminic Agents; Nor Is It Attenuated By Sympmentioning

confidence: 99%

Pathogenesis of Cardiovascular Alterations in Dogs Treated with Minoxidil

et al. 1989

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Minoxidil and other potent vasodilators cause coronary arterial injury, right atrial hemorrhagic lesions, and subendocardial necrosis in dogs, This paper discusses the pathogenesis of coronary arterial and right atrial lesions associated with minoxidil in the dog, Acute coronary vascular injury characterized by segmental medial hemorrhage and necrosis and perivascular inflammation occurred only during the first few days of treatment, after which tolerance to further acute injury developed, At 30 d or more of treatment, coronary vascular injury was characterized by perivascular fibrosis rarely attended by medial distortion or hyperplasia and subintimal thickening, changes consistent with responses to previous injury, Right atrial hemorrhagic lesions, unlike coronary vascular injury, often became progressively more extensive with continued treatment. At 3 d, atrial hemorrhage and inflammation were confined to the subepicardium ofthe right atrium, evidently around affected subepicardial branches of the right coronary artery, At 30 d, fibrovascular proliferative right atrial lesions (granulation tissue with evidence of continual hemorrhage) extended from the epicardium to the myocardium, with eventual replacement ofthe atrial wall by mature connective tissue at I yr of treatment. Minoxidil-induced cardiovascular lesions were not prevented by treatment with a l3-blocker (propranolol), or an a-blocker (dibenzylene), or by sympathetic neural activity suppression (surgical sympathectomy or constant carotid sinus nerve stimulation), suggesting that the sympathetic response to the pharmacologic activity of minoxidil was not responsible for the induction of the cardiovascular lesions. Minoxidil-related vascular lesions were confined to the most pharmacologically responsive segment of the arterial system, the coronary arteries, suggesting that medial injury may have been associated with tensile changes in the arterial wall.

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“…Whereas the adrenergic-blocking drugs, methyldopa (1) and propranolol (2) reduce PRA, vasodilator antihypertensives such as diazoxide (3), hydralazine (4), and sodium nitroprusside (5) increase PRA in hypertensive patients. The new potent antihypertensive vasodilator, minoxidil, has been shown to increase PRA in the rat (6) and in patients with hypertension (7,8). Minoxidil-induced increase in PRA may be attributable to any one of three known pharmacological effects of the drug: decrease in arterial pressure, reflex increase in sympathetic tone (7), or decrease in sodium excretion rate (8,9).…”

Section: Introductionmentioning

confidence: 99%

“…The new potent antihypertensive vasodilator, minoxidil, has been shown to increase PRA in the rat (6) and in patients with hypertension (7,8). Minoxidil-induced increase in PRA may be attributable to any one of three known pharmacological effects of the drug: decrease in arterial pressure, reflex increase in sympathetic tone (7), or decrease in sodium excretion rate (8,9). The present study was undertaken to assess the relative roles of these three variables in the genesis of minoxidilinduced increase in PRA in patients with essential hypertension.…”

Section: Introductionmentioning

confidence: 99%

Control plasma renin activity and changes in sympathetic tone as determinants of minoxidil-induced increase in plasma renin activity.

O’Malley¹,

Velasco²,

Wells³

et al. 1975

J. Clin. Invest.

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A B S T R A C T A study was made of the possible mechanism(s) underlyingminoxidil-induced increase in plasma renin activity (PRA). 10 patients with essential hypertension were treated with minoxidil and subsequently with a combination of minoxidil plus propranolol.Minoxidil lowered mean arterial pressure 31.6±3.3 mm Hg, mean ±SEM. There was an associated increase in both PRA, 6.26+2.43 ng/ml/h, and heart rate, 21.4±2.7 beats/min. The changes in PRA and heart rate were positively correlated, r, 0.79. Addition of propranolol reduced mean arterial pressure by a further 10.1+±1.5 mm Hg and returned heart rate to control levels. Propranolol reduced PRA significantly but not to control levels. Control PRA positively correlated with PRA on minoxidil, r, 0.97, and with PRA on minoxidil plus propranolol, r, 0.98. We conclude that control PRA is a major determinant of change in PRA with minoxidil.Minoxidil increased PRA by at least two mechanisms: (a) an adrenergic mechanism closely related to change in heart rate and blocked by propranolol, and (b) a mechanism (s) not sensitive to propranolol and possibly related to decrease in renal perfusion pressure.

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Minoxidil—an alternative to nephrectomy for refractory hypertension

Cited by 25 publications

References 0 publications

Plasma concentration and acetylator phenotype determine response to oral hydralazine.

Plasma concentration and acetylator phenotype determine response to oral hydralazine.

Pathogenesis of Cardiovascular Alterations in Dogs Treated with Minoxidil

Control plasma renin activity and changes in sympathetic tone as determinants of minoxidil-induced increase in plasma renin activity.

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