Treatment of hypertension with nifedipine, a calcium antagonistic agent.

Olivari, Maria Teresa; Bartorelli, C; Polese, A; Fiorentini, Cesare; Moruzzi, P; Guazzi, Maurizio D.

doi:10.1161/01.cir.59.5.1056

Cited by 341 publications

(63 citation statements)

References 18 publications

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“…However, they contrast with the results reported by Olivari et al 13 and Leonetti et al, 14 using a single 10-mg oral dose of nifedipine, Guazzi et al, 15 using oral nifedipine (10 mg q.i.d.) administration for 1 week, and Bruun et al, 16 using a mean 51 mg/day oral dose of nifedipine for 12 weeks.…”

Section: Side Effectsmentioning

confidence: 65%

Effect of nifedipine on renal function in patients with essential hypertension.

et al. 1988

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SUMMARY Twenty-six essential hypertensive patients were entered into a protocol to assess the blood pressure and renal effects of the dihydropyridine calcium antagonist nifedipine (30-120 mg/day given in divided doses) administered for 4 weeks. Nifedipine monotherapy effectively lowered blood pressure in 73% of the patients. Glomerular filtration rate and effective renal plasma flow were increased 13.3 and 19.6%, respectively. The filtration fraction and urinary albumin excretion remained unchanged. Renal vascular resistance was markedly reduced (25.2%). Changes observed in renal function were independent of the patients' initial glomerular filtration rate. 1 ' 2 The potential role for calcium antagonists to reverse or prevent the pathophysiological progression of hypertensive renal disease or to attenuate the progression of chronic renal disease is unknown.We have previously reported on the renal effects of the benzothiazepine calcium antagonist diltiazem 3 * and the dihydropyridine calcium antagonist amlodipine.3 These studies suggested that calcium antagonists have the potential to enhance effective renal plasma flow (ERPF) and renal blood flow, to preserve or Received August 24, 1987; accepted December 3, 1987. improve glomerular filtration rate (GFR), and to lower renal vascular resistance. We now report on the shortterm renal effects of the dihydropyridine calcium antagonist nifedipine. Our results suggest that renal function abnormalities encountered in the essential hypertensive state may be improved by nifedipine independently of its systemic blood pressure effect.Patients and Methods Twenty-six patients with essential hypertension were selected for this prospective study. To be included, each patient had to maintain a mean 5-minute recumbent diastolic blood pressure (fifth phase) between 95 and 114 mm Hg following withdrawal of prior drug therapy and during 2 to 4 weeks of placebo therapy. The diagnosis of essential hypertension was established by history and physical examination and by the absence of clinical findings suggestive of a secondary form of hypertension. Excluded from the study were patients with a history or clinical or laboratory findings of moderate to severe cardiomegaly, congestive heart failure, recent myocardial infarction, second-or thirddegree heart block, overt diabetes mellitus, or Grade 3 or 4 Keith-Wagener hypertensive retinopathy, as well as patients who were nonadherent to drug therapy (as monitored by count of returned tablets).

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Section: Side Effectsmentioning

confidence: 65%

Effect of nifedipine on renal function in patients with essential hypertension.

et al. 1988

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“…The development of drugs that interfere with the entry of calcium into cells and thus relax vascular smooth muscles (Fleckenstein, 1977) has provided the clinician with new therapeutic agents potentially of considerable value in the treatment of hypertension (Lewis et al, 1978;Olivari et al 1979).…”

Section: Discussionmentioning

confidence: 99%

Blood pressure, heart rate and A‐V conduction responses to nicardipine in hypertensive patients receiving atenolol.

Kolloch¹,

Stumpe²,

Overlack³

1985

Brit J Clinical Pharma

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1 The antihypertensive effect of the combined use of the new calcium channel blocker nicardipine and atenolol was assessed in a double-blind, placebo-controlled trial involving twenty hypertensive patients. 2 Atenolol 100 mg once daily was given to all patients. In addition, either placebo or nicardipine, in increasing doses (5-20 mg three times daily), was allocated randomly to the patients. 3 Compared with placebo, nicardipine had an additional dose-dependent, blood-pressurelowering effect in the hypertensive patients who had been pretreated with atenolol. An increase in the heart rate was not observed, suggesting that atenolol prevented reflex activation of sympathetic nerve tone caused by the vasodilating properties of nicardipine. 4 The combination of both atenolol and nicardipine was well tolerated by all patients; side effects were minor and did not cause discontinuation of the treatment. No effects on A-V conduction were observed. 5 It is concluded that the combined administration of nicardipine and atenolol is a useful treatment for hypertension that is well accepted by the patients.

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“…Calcium channel blockers act as vasodilators, thereby reducing blood pressure (Lewis et al, 1978;Olivari et al, 1979). The reduction in blood pressure that occurs with some calcium antagonists seems to correlate with the level of pre-treatment plasma renin activity (PRA) and the age of the patient (Buhler et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Nicardipine hydrochloride in essential hypertension‐a controlled study.

Asplund¹

1985

Brit J Clinical Pharma

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Fifty patients with mild essential (primary) hypertension entered a double‐blind, parallel‐group study with either nicardipine 30 mg three times daily or placebo, randomly assigned as monotherapy for 6 weeks. At the end of 6 weeks, the nicardipine‐treated group had a statistically significant reduction in mean supine systolic/diastolic pressure of 21.2/15.0 mm Hg (P less than 0.001) compared with the nonsignificant reduction of 0.7/2.9 mm Hg in the placebo‐treated group. The difference in mean response between the nicardipine‐ and placebo‐ treated groups was significant (P less than 0.001). In the nicardipine‐ treated group, the reduction in mean standing systolic/diastolic blood pressure, 17.9/13.8 mm Hg, was significant (P less than 0.001), whereas in the placebo‐treated group the change was +3.0/‐1.5 mm Hg. The difference between the two treatment groups was significant (P less than 0.001). In both treatment groups, changes in pulse rate were minor, and there was no evidence of tachyphylaxis occurring with nicardipine. Adverse experiences were minor in all cases except for one patient with muscle pain during treatment with nicardipine. Patients who received nicardipine showed a mean increase of 52% in plasma renin activity (PRA) after 6 weeks (P less than 0.01). Initial basal or stimulated PRA did not correlate with blood pressure reduction on nicardipine. Nicardipine 30 mg three times daily is a well‐tolerated and effective antihypertensive agent.

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Treatment of hypertension with nifedipine, a calcium antagonistic agent.

Cited by 341 publications

References 18 publications

Effect of nifedipine on renal function in patients with essential hypertension.

Effect of nifedipine on renal function in patients with essential hypertension.

Blood pressure, heart rate and A‐V conduction responses to nicardipine in hypertensive patients receiving atenolol.

Nicardipine hydrochloride in essential hypertension‐a controlled study.

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