Disease relevance of Rogaine

• Reversal of baldness in patient receiving minoxidil for hypertension [1].
• Minoxidil treatment of malignant hypertension. Recovery of renal function [2].
• Two are presently doing well, while one died of causes unrelated to uremia or minoxidil therapy [2].
• In studies with normotensive rats, propranolol impaired renin release and tachycardia resulting from hydralazine and minoxidil and potentiated their hypotensive action [3].
• Minoxidil for male-pattern baldness [4].

Psychiatry related information on Rogaine

• A total of 21 patients received 2% minoxidil for treatment of erectile dysfunction with instructions to apply 1 cc of the solution slowly over the glans penis 20 minutes before intercourse [5].
• Finally, the prevention of minoxidil-induced amnesia in the mouse by B25 and related benzylamines, comparable to the same effect shown by TEA and 4-AP, indicates that these compounds are endowed with potential pharmacological activity in the CNS as well [6].
• We evaluated the antihypertensive efficacy of "once-a-day" minoxidil, given in conjunction with a diuretic and sympatholytic, and the effect of this simple regimen on patient compliance [7].
• Most cases are associated with malignant tumors or non-malignant condition such as porphyria cutanea tarda, AIDS, anorexia nervosa, thyrotoxicosis, or secondary to topical or systemic drugs (e.g. cyclosporine, phenytoin, diazoxide, minoxidil) [8].

High impact information on Rogaine

• Good blood pressure control was obtained in 21 (72%) of 29 patients when minoxidil was given in dosages up to 40 mg/day [9].
• Pericardial effusions associated with minoxidil [10].
• Minoxidil in breast milk [11].
• Thrombocytopenia and minoxidil [12].
• When they become available, two investigational drugs, minoxidil and an oral converting enzyme inhibitor, both of which lower total peripheral resistance, will offer a new approach to controlling truly resistant hypertension [13].

Chemical compound and disease context of Rogaine

• In the presence of moderate to severe diastolic hypertension, hydralazine, captopril, and minoxidil may have value, but such potent agents should generally be avoided with isolated systolic hypertension [14].
• These results show that in patients with severe left ventricular hypertrophy, captopril-based triple therapy reduces left ventricular mass without altering systolic performance, whereas minoxidil-based therapy does not [15].
• In the remainder, minoxidil, nadolol, and a diuretic were begun simultaneously because of severe hypertension [16].
• In a double-blind 6 month trial, the cardiac effects of captopril and minoxidil, administered as third step treatments, were compared in 34 men with essential hypertension and diastolic blood pressure greater than 95 mm Hg who were taking 200 mg/day of metoprolol and 80 mg/day of furosemide [15].
• Felodipine as a replacement for minoxidil in the treatment of severe hypertension [17].

Biological context of Rogaine

• In one patient, diastolic blood pressure remained unchanged (120 mm Hg) despite 60 mg of minoxidil and volume depletion [18].
• Heart rate rose slightly, from 85.4 +/- 2.9 to 90.9 +/- 3.2 beats/min, after minoxidil (p less than 0.02) and mean arterial pressure fell slightly, from 88.0 +/- 2.3 to 84.9 +/- 2.5 mm Hg (p less than 0.05) [19].
• Cardiac volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats [20].
• Mean systemic arterial pressure, cardiac output, and pulmonary artery pressure were then compared before and after the addition of acute (5 day) and chronic (2 month) therapy with minoxidil [21].
• Minoxidil did not affect right atrial, pulmonary arterial and pulmonary wedge pressures [19].

Anatomical context of Rogaine

• Suppression of fibroblast proliferation and lysyl hydroxylase activity by minoxidil [22].
• Prolonged treatment with minoxidil induced significant increases in left ventricular internal diameter, as well as in left and right ventricular weights, but not in the wall thickness of the left ventricle [23].
• Significant increases in sulfotransferase activity toward two P-PST-specific substrates, minoxidil and 4-nitrophenol, were detected in cytosol prepared from COS-7 cells transfected with P-PST-1 in the expression vector p-SV-SPORT-1 [24].
• These studies show that sulfation is a critical step for hair-growth effects of minoxidil and that it is the sulfated metabolite that directly affects hair follicles [25].
• Effect of minoxidil on cultured keratinocytes [26].

Associations of Rogaine with other chemical compounds

• These observations suggest that chronic reduction of impedance to left ventricular ejection with minoxidil or hydralazine is possible in patients with severe intractable heart failure and deserves further clinical trial [27].
• Although an arterial vasodilator (minoxidil) resulted in significant pulmonary vasodilation during harvest, it lacked other nonvasodilating effects of PGE1 and resulted in poor preservation [28].
• Minoxidil or minoxidil in combination with 2.5 mg glyburide resulted in a similar significant decrease in blood pressure compared with the response to glyburide alone [29].
• In a double blind crossover trial blood pressure on felodipine (150/88 +/- 19/8 mmHg, SD) was the same as on minoxidil (148/87 +/- 23/11 mmHg, NS) and the postural difference was similar (NS) on both drug regimens [17].
• Blood pressure was adequately controlled only after progressively more intensive drug regimens, finally including minoxidil, nadolol, and furosemide [30].

Gene context of Rogaine

• Platelet TL PST assayed with minoxidil showed thermal stability and a response to DCNP that were essentially the same as TL PST [31].
• It was also demonstrated that cDNA encoded human liver dehydroepiandrosterone sulfotransferase and estrogen sulfotransferase contributed to the sulfation of minoxidil [32].
• We thus speculated that activation of PGHS-1 might be a mechanism by which minoxidil (2,4-diamino-6-piperidinopyrimidine-3-oxyde) stimulates hair growth in vivo [33].
• Thus, DHEA ST activity must be considered when determining the human tissue sulfotransferase contribution to minoxidil sulfation [34].
• Characterization of recombinant human liver dehydroepiandrosterone sulfotransferase with minoxidil as the substrate [34].

Analytical, diagnostic and therapeutic context of Rogaine

• We treated eight severely hypertensive, long-term hemodialysis patients who failed to respond to ultrafiltration or conventional medication with minoxidil rather than with bilateral nephrectomy [2].
• Despite the possibility of adverse reactions, minoxidil is indicated in patients whose blood pressure cannot be controlled with conventional therapy, in persons with major adverse reactions to other drugs, and in patients who are candidates for bilateral nephrectomy for control of hypertension [35].
• Concomitant with the initiation of minoxidil treatment, ECG changes consisting of flattening or inversion of the T waves, ranging from slight to very marked, were observed in 90% of the patients [36].
• Hair growth effects of oral administration of finasteride, a steroid 5 alpha-reductase inhibitor, alone and in combination with topical minoxidil in the balding stumptail macaque [37].
• Thirteen patients whose hypertension had been resistant to conventional drug therapy, had minoxidil added to their regimen in doses from 5 to 60 mg/day [38].

References