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

The influence of a 6-week treatment of female Wistar rats with one-kidney, one clip (1-K, 1 C) renal hypertension, with the calcium antagonist nifedipine on plasma volume, red cell Na+ handling and plasma atrial natriuretic peptide immunoreactivity (ANP-IR) was studied. Measurements were performed at 2 and 6 weeks after surgery. In 1-K, 1 C rats plasma volume was increased and red cell Na+ pump activity was reduced only after 2 weeks. Blood pressure, heart weights and plasma ANP were massively increased after both 2 and 6 weeks. 1-K, 1 C-rats treated with nifedipine had normal plasma volume, plasma ANP, and red cell Na+ pump activity in comparison with sham-operated rats. Increases in blood pressure and heart weights were attenuated. It is concluded that 1-K, 1 C hypertension in the rat is associated with cardiomegaly, rise in plasma ANP, initial hypervolemia and depression of the membrane Na+ pump. Nifedipine prevents the occurrence of hypervolemia and secondary phenomena such as rises in plasma ANP and cardiomegaly. This may play an important contributory role in the prevention of pathological sequelae.
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PMID:Modulation by chronic nifedipine of plasma atrial natriuretic peptide, cell Na+ transport and plasma volume in rats with renal hypertension. 284 89

Calcium-entry blocking agents resemble established dilators such as diazoxide, minoxidil and hydralazine in that they act predominantly on the arterial resistance vessels and have little or no effect upon the veins. They have therefore been evaluated in the treatment of hypertension. Controlled studies have shown that verapamil and nifedipine are effective in decreasing blood pressure when given as sole agents. The antihypertensive effect of nifedipine is additive with that of a beta blocker, and nifedipine is also effective when given as a "third step" agent in combination with a beta blocker (or alpha methyldopa) and a diuretic. In contrast to other directly acting dilators, nifedipine causes, at most, only moderate stimulation of renin secretion and verapamil does not increase renin release at all; neither drug induces sodium retention. Both verapamil and nifedipine produce a moderate incidence of unwanted effects; these are mostly subjective in nature, but verapamil may cause constipation that is occasionally severe and nifedipine sometimes causes ankle swelling. Calcium-entry blockers should be considered as initial therapy when some contraindication exists to the use of other standard drugs. Nifedipine appears preferable to hydralazine for use in combination with a beta blocker and a diuretic: it is at least as effective as hydralazine and has a lower incidence of serious adverse effects.
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PMID:Calcium-entry blocking agents in the treatment of systemic hypertension. 285 16

A randomized cross-over trial was undertaken on 21 occupationally active persons who had a stable mild or moderate hypertension with the purpose of comparing the effect of a beta-adreno-receptor blocking agent (atenolol) with that of a calcium channel inhibitor (nifedipine). The doses recommended by the manufactures were used. Atenolol (100 mg) given once a day resulted in a marked hypotensive effect at rest as well as during exercise, the compliance was satisfactory, and the hemodynamic changes were not reflected in unfavourable side effects during muscular exercise or in the subjects own personal assessment of fatigue during the exercise tests which ranged in energy expenditure from about three to six times the resting level. However, unfavourable, modest side effects occurred in two subjects during atenolol medication to the extent that they wanted to terminate the study. Nifedipine therapy with doses of 10 mg, three times a day, resulted in a modest, but statistically insignificant reduction in arterial blood pressure, which contrasts with previous published results. It is suggested that the modest effect is caused or related to the poor compliance and a daily dose that was quantitatively too small. No unfavourable side effects were seen during muscular efforts when the subjects were on nifedipine medication.
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PMID:Working ability and exercise tolerance during treatment of a mild hypertension. I. Comparison between a beta-adreno-receptor blocking drug and a calcium antagonist. 286 20

Results are presented from a study conducted in twelve male patients with hypertension who were treated during alternating one-month periods with a calcium channel blocker, a beta blocker, or a combination of both drugs. After one month of placebo therapy, the patients received 10 mg of nifedipine three times daily, 100 mg of metoprolol twice daily plus 10 mg of nifedipine three times daily, or 100 mg of metoprolol twice daily during successive periods. Nifedipine monotherapy resulted in a significant decrease in both systolic and diastolic blood pressures at rest and in systolic blood pressure during exercise. Monotherapy with metoprolol also significantly reduced systolic blood pressure during exercise. Combination therapy with the calcium channel blocker and the beta blocker produced a significantly greater decrease in both resting and exercise blood pressures than with either drug alone, with achievement of adequate blood pressure control in all patients.
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PMID:Nifedipine in combination therapy for chronic hypertension. A review. 286 57

The hypotensive effect of vasodilator monotherapy in hypertension is attenuated by a baroreceptor-mediated increase in the sympathetic release of noradrenaline. Nifedipine induces a rise in noradrenaline release, but it is not known to affect noradrenaline-induced vascular contraction of smooth muscle to a clinically significant degree. The haemodynamic and hormonal effects of a single sublingual dose of nifedipine 20 mg in 8 moderately hypertensive patients have been studied before and during postsynaptic alpha 1-blockade with prazosin. The antihypertensive effect of nifedipine was significantly increased by prazosin pretreatment (fall in mean arterial pressure 60 min after nifedipine: -16.7% with and -8.5% without prazosin), despite similar increases in plasma noradrenaline. Prazosin alone caused no change in supine blood pressure for 2 h after an oral dose of 2 mg. The findings are in keeping with the hypothesis that prazosin blocks a compensatory reaction to vasodilatation caused by nifedipine.
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PMID:The influence of alpha 1-adrenergic blockade on the acute antihypertensive effect of nifedipine. 286 64

Nifedipine is known to reduce blood pressure both acutely and chronically. However, the following questions remain to be answered: can nifedipine be given acutely and safety to patients with severe hypertension in an outpatient setting, would its efficacy be retained with long-term therapy, and is nifedipine safe in the presence of cardiomegaly? Nifedipine (10 mg capsule sublingually) was given to 46 outpatients with severe or apparently refractory hypertension; 19 were followed-up for 18 months and 18 for 24 months. Nifedipine reduced blood pressure acutely and safely in 43 of 46 outpatients (mean control diastolic pressure 137 mm Hg), irrespective of prior treatment regimen. Blood pressure levels after 2 to 24 months of twice daily oral nifedipine (10 mg) were similar to 20-minutes levels, showing that tolerance did not occur. In a separate series of 37 patients, who had radiologic cardiomegaly in addition to hypertension, the control ejection fraction was 62%. Nifedipine, when used acutely, slightly increased the ejection fraction to 65% (p less than 0.005). Our studies show that in outpatients with severe hypertension, sublingual nifedipine is an antihypertensive agent which acts swiftly and safely, without causing a decrease in the ejection fraction when it is used for acute blood pressure reduction, and that subsequent therapy with oral nifedipine results in a predictive long-term hypotensive effect.
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PMID:Acute effect of nifedipine on blood pressure and left ventricular ejection fraction in severely hypertensive outpatients: predictive effects of acute therapy and prolonged efficacy when added to existing therapy. 286 72

Because we so rarely know the cause of hypertension, antihypertensive therapy remains empiric. However, certain principles of treatment are emerging; one of these concerns the critical role of the kidney in antihypertensive therapy. Whether or not the kidney is primarily responsible for hypertension in a patient, it is the patient's renal response to treatment that determines, to a major degree, an agent's efficacy. Vasodilators have been a conceptually attractive approach to the treatment of high blood pressure, because they decrease total peripheral resistance, which is considered to be the mechanism responsible for this condition in most patients. Nonspecific vasodilators exert a series of actions on the kidney--including profound sodium retention and reactive renin release--that limits therapeutic response. For reasons that are not yet clear, but are apparently related to specific action on calcium entry into vascular smooth muscle, endocrine function, and renal hemodynamics, calcium channel blocking agents, such as nifedipine, have an advantage in the treatment of hypertension. They cause little or no sodium retention; thus, the addition of a diuretic agent is not required. In fact, there is evidence that sodium loading in certain patients may potentiate the antihypertensive efficacy of these drugs. The renin-angiotensin system seems to be activated to a somewhat lesser degree by calcium channel blocking agents than it is by nonspecific vasodilators; in addition, these agents interfere with the actions of angiotensin on aldosterone release. Moreover, their dilator action on the renal blood supply favors sodium excretion. Nifedipine either has no effect on the renal blood supply or induces an increase in renal blood flow and maintains glomerular filtration rate, both of which combine to support the ensuing natriuresis.
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PMID:Strategies in antihypertensive therapy: implications of the kidney. 287 43

1. Ketanserin or slow-release nifedipine were added to the treatment of 24 patients with hypertension uncontrolled by a thiazide diuretic plus beta-adrenoceptor antagonist in an observer-blind, randomised parallel-group study of 6 months duration. 2. At 6 months the mean falls in supine blood pressure were for ketanserin (mean daily dose 77 mg) 7/5 mm Hg and for nifedipine (mean daily dose 62 mg) 27/10 mm Hg. The difference between the treatments was significant for systolic blood pressure (P less than 0.02) and mean arterial pressure (P less than 0.05). Six nifedipine-treated patients reached target blood pressure, compared with one patient with ketanserin (P less than 0.02). 3. One patient taking nifedipine, and none taking ketanserin withdrew because of side-effects. The tolerability of the two drugs was broadly similar. 4. Ketanserin treatment was associated with significant changes in supine pulse rate (-8 beats min-1, P less than 0.05) and corrected QT interval (+27 ms, P less than 0.05). Nifedipine treatment had no effect on these variables. The change in pulse rate was significantly different between the groups. 5. In patients treated with a diuretic and beta-adrenoceptor blocker who required additional treatment ketanserin was significantly inferior to nifedipine.
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PMID:Comparison of ketanserin and slow-release nifedipine added to the treatment of hypertensive patients uncontrolled by a thiazide diuretic plus beta-adrenoceptor blocker. 289 36

Nifedipine slow release tablets were substituted for minoxidil in the treatment of 13 patients with hypertension refractory to conventional therapy. In 12 patients substitution was associated with continuing control of blood pressure (BP), although 11 required maximum dose of 120 mg daily and one 80 mg daily. BP control remained satisfactory in nine patients for at least one year after substitution and in all, loop diuretics previously required with minoxidil to control fluid retention, were discontinued. Three patients (23%) however had to be withdrawn because of side effects; one within days of starting therapy and two after three months: one patient died after sustaining myocardial infarction. There was no evidence of deterioration in renal function in those patients continuing on nifedipine. This drug in combination with other antihypertensive agents provides an alternative approach to the management of patients with refractory hypertension, avoiding the severe side effects of the potent vasodilators.
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PMID:Nifedipine substituted for minoxidil in the treatment of refractory hypertension. 290 71

Fifty-one patients with urgent hypertension were treated in the emergency department with either oral nifedipine or oral clonidine in a randomized double-blind prospective study. Nifedipine was administered as a single dose of 20 mg. Clonidine was administered as an initial dose of 0.1 mg with hourly doses of 0.1 mg. Nifedipine was successful in reducing diastolic blood pressure in 83% of the patients within 45 minutes and in 96% of the patients within two hours, with a mean reduction in systolic blood pressure of 47 mm Hg and diastolic blood pressure of 29 mm Hg. Thirty percent of those who initially responded to nifedipine experienced a subsequent increase in diastolic blood pressure to pretreatment levels within three hours. Clonidine was successful in reducing diastolic blood pressure in 79% of the patients within four hours, with a mean reduction in systolic blood pressure of 51 mm Hg and diastolic blood pressure of 30 mm Hg. Our results indicate that both nifedipine and clonidine are safe and effective in the treatment of urgent hypertension. Nifedipine had a much more rapid onset of action with a greater initial success rate, and it was free from the sedative side effects of clonidine. We believe that either nifedipine or clonidine may be used as first-line therapy in the treatment of urgent hypertension.
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PMID:Oral nifedipine vs oral clonidine in the treatment of urgent hypertension. 231 Feb 88


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