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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Minoxidil is a potent antihypertensive drug widely used in severe arterial hypertension and in that refractory to treatment. Its effectiveness in less severe forms of hypertension was evaluated in 15 patients who had either a severe to moderate arterial hypertension not previously treated, or who did not tolerate the side effects of other antihypertensive drugs. The usefulness of methyldopa and chlortalidone to prevent a potential minoxidil-induced tachycardia and fluid retention, respectively, was also tested. The patients were initially treated with chlortalidone 100 mg/day, and methyldopa 500 mg/day. Minoxidil was then given in increasing doses until the diastolic blood pressure was equal to or inferior to 90 mmHg. This occurred consistently at doses which ranged from 5 to 50 mg/day (average, 29 mg). Treatment with minoxidil was continued for four months; tolerance to the drugs was not observed. Low doses of methyldopa and chlortalidone were effective in controlling the tachycardia and the retention of sodium and water induced by minoxidil. The three associated drugs were well tolerated and the life quality improved in most patients. Hypertrichosis was the most consistent side effect. Two patients were withdrawn from the study after the blood pressure was controlled by minoxidil, because of the appearance of angor in one, and edema and heart failure in the other.
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PMID:Minoxidil in severe and moderately severe hypertension, in association with methyldopa and chlortalidone. 713 53

Minoxidil was used by 27 investigators for the treatment of severe refractory hypertension which had failed to respond to extensive multiple therapy. Blood pressure was controlled in 71 of 101 patients. The most common side effects were fluid retention and hypertrichosis. In 71% of patients the drug was withdrawn because of intolerance.
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PMID:Minoxidil experience in Australia 1974-1980. 725 11

Minoxidil, a potent peripheral vasodilator, was used concomitantly with other antihypertensive drugs for severe hypertension in three children for 47 to 158 weeks at the dosage of 40 to 50 mg/day. Two patients had three and two courses of minoxidil, respectively. Attempts were made to withdraw minoxidil in all children because of severe hypertrichosis. Minoxidil was withdrawn over periods varying from four to 12 weeks. Rebound hypertension manifesting as hypertensive encephalopathy occurred in all when minoxidil was withdrawn rapidly. The occurrence of rebound hypertension correlated with the total cumulative dose of minoxidil in mg/kg/week given prior to the withdrawal (P less than 0.05) and the rapidity (four to eight weeks) with which minoxidil was withdrawn (P less than 0.05), but not with the total duration of therapy, duration at maximal dosage, or the amount of minoxidil in mg/kg on the day prior to withdrawal. Rebound hypertension also did not occur when minoxidil was withdrawn gradually (12 weeks) or if the patient was receiving a small dose (2.5 to 5 mg/day). Pretreatment with an alpha-blocking agent (prazosin) or the discontinuation of the concomitantly administered beta-blocker (propranolol) prior to the withdrawal seemed to prevent rebound hypertension. We suggest that the dosage of minoxidil should be decreased very gradually.
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PMID:Rebound hypertension following minoxidil withdrawal. 735 90

Minoxidil is an extremely potent hypotensive drug. Good control of refractory hypertension can be achieved without major side effects by using small to moderate doses in combination with other drugs. In particular, minoxidil and labetalol are effective when they are used with frusemide.
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PMID:Minoxidil and labetalol: very effective antihypertensive combination. 737 68

Minoxidil (6-amino-1,2-dihydro-1-hydroxy-2-imino-4-piperidinopyrimidine), a new substance for the treatment of severe hypertension, is frequently associated with hypertrichosis. This side effect may spontaneously disappear despite continuation of minoxidil-treatment, as it is demonstrated in this case-report.
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PMID:[Hypertrichosis caused by minoxidil]. 739 13

Minoxidil was administered to 13 patients with arterial hypertension resistant to ordinary antihypertensive drugs and with various degrees of renal failure. Four patients were followed in this way for 50 weeks. Blood pressure values fell from 208 +/- 9.8/124 +/- 4.8 to 153.1 +/- 7.8/86.9 +/- 2.6 at the end of the treatment period. Propanolol and furosemide were used to offset sodium retention and reflex tachycardia. There was no decrease in renal function. In patients examined for the longest period, the minoxidyl dose, after an intermediate reduction stage, reached the 8th week value. Hypertrichosis was the most disturbing side-effect, especially for the female patients. The question of pericarditis is discussed.
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PMID:[Treatment of arterial hypertension with minoxidil in renal insufficiency]. 743 94

A detailed study has been made of the five hypertensive patients who received Minoxidil in Dumfries; four have been observed for over a year. Minoxidil was found to be highly effective, free from commonly encountered side effects and capable of achieving excellent control of blood pressure when given once daily. Its use led to simpler drug regimens, improved compliance and significant reduction in the length, or even need, of admission to hospital. A prolonged and clinically useful delay in the recurrence of hypertension following withdrawal of the drug was also observed.
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PMID:Advantages of treatment of hypertension with Minoxidil. 745 78

Minoxidil, in addition to its effect on hypertension and hair growth, has been proposed as a potential antifibrotic agent. Minoxidil inhibits the contraction of collagen lattices by human fibroblasts in vitro. However, the mechanism of inhibition is unknown. As minoxidil is metabolised in the body to minoxidil glucuronide and minoxidil sulphate, we investigated the potencies of these metabolites to inhibit collagen lattice contraction. We also studied selected analogues of minoxidil to assess the influence of certain functional groups in the inhibition. The major metabolite, minoxidil glucuronide, proved to be inactive, whereas minoxidil sulphate was considerably more active than minoxidil. In terms of the structural analogues, the substitution of one amino group by a methyl group resulted in loss of the inhibitory activity; removal of the nitroxide oxygen led to stronger inhibition than with minoxidil. Further studies are planned to learn more about a possible role for minoxidil in wound contraction.
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PMID:The effect of minoxidil analogues and metabolites on the contraction of collagen lattices by human skin fibroblasts. 773 78

Minoxidil is a potent antihypertensive agent used in the treatment of resistant hypertension. A case is presented which illustrates a probably fatal interaction between minoxidil and a coagulation disorder.
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PMID:Minoxidil, hypercoagulability and thromboembolic disease of the lung. 873 32

Chronic treatment with minoxidil induces cardiac trophic and sympathetic responses, which may increase the propensity for lethal arrhythmias. To test this hypothesis, acute coronary artery occlusion was performed in conscious normotensive rats treated for 2 or 5 weeks with minoxidil with the use of a 2-stage approach to cause a myocardial infarction. For comparison, rats with aortocaval (A-V) shunts and spontaneously hypertensive rats (SHR) were studied. Minoxidil increased left ventricular and right ventricular weights by 15% to 20%, and the A-V shunt increased these weights by 30% to 40%. In SHR, left ventricular weight was increased by 50%, and right ventricular weight was increased by 25%. In rats treated with minoxidil for 5 weeks, coronary artery occlusion caused a rapid and marked mortality, and 4 hours after myocardial infarction, only 18% of these rats were alive versus 61% of the control rats. In rats with the A-V shunt, coronary artery occlusion was also associated with increased mortality, and after 6 hours, 33% were still alive compared with 59% of the control rats. In contrast, SHR with marked hypertension and cardiac hypertrophy showed only a minor increase in mortality (survival rates were 53% versus 60% in SHR versus Wistar-Kyoto rats, respectively). Mortality was preceded by high arrhythmia scores, and ventricular fibrillation was the cause of death. Discontinuation of minoxidil for 1 week, sympathetic blockade with nadolol or clonidine, or blockade of the renin-angiotensin system with enalapril or losartan did not improve minoxidil-induced excess mortality. We conclude that ventricular stretch and other mechanisms (eg, cardiac vagal activity) in rats appear to be more potent than hypertension-induced left ventricular hypertrophy in predisposing for lethal arrhythmias in the setting of acute ischemia.
Hypertension 2001 Feb
PMID:Mortality after coronary artery occlusion in different models of cardiac hypertrophy in rats. 1123 Feb 73


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