Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 72-year-old woman with 5-year history of essential hypertension developed peritoneal tuberculosis. The patient's hypertension, which had been well-controlled by long-acting nifedipine, deteriorated after the administration of rifampicin, an antitubercular agent. During use of nifedipine and rifampicin, both the peak plasma concentration and the area under the curve of nifedipine decreased markedly to about 40% of those without rifampicin. The findings suggest that rifampicin may increase the elimination of nifedipine, presumably by induction of its hepatic metabolism. Nisoldipine, another calcium antagonist, also failed to lower the patient's blood pressure, when given in combination with rifampicin. Taken together, these findings indicate that more caution should be urged when calcium antagonist is prescribed along with rifampicin.
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PMID:Case report: nifedipine-rifampicin interaction attenuates the effect on blood pressure in a patient with essential hypertension. 134 93

The antihypertensive effect of nisoldipine on ambulatory blood pressure was investigated using continuous noninvasive monitoring in 12 patients with moderate essential hypertension. Treatment with nisoldipine 5 mg twice a day for 2 weeks resulted in a decrease in the average of each patient's mean arterial pressure for the whole day from 110.3 +/- 6.8 to 103.2 +/- 8.8 mm Hg (P = 0.0007). This decrease in mean arterial pressure was due to a decrease in both systolic and diastolic pressures. The reduction in blood pressure was most marked at the time of the originally high blood pressure readings. Comparisons of consecutive means of 2-hourly mean arterial pressure readings showed a statistically significant effect from 6:00 AM to midnight. Blood pressures between midnight and 6:00 AM were similarly low, before and during nisoldipine therapy. There was no change in heart rate. Untoward symptoms were reported with similar frequency, and of similar severity, both before and during therapy. Nisoldipine 5 mg twice a day is an effective antihypertensive agent, reducing moderately elevated blood pressure in ambulatory, working patients with essential hypertension. At the dosage used, it had no demonstrable effect on heart rate and minimal, if any, side effects.
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PMID:Effect of nisoldipine on ambulatory blood pressure under 24-hour noninvasive monitoring. 139 98

This randomized double-blind parallel group study characterized the pharmacokinetics of the calcium channel antagonist, nisoldipine (core-coat tablets), administered once daily for 7 days in doses of 5 mg (n = 12), 10 mg (n = 13), 20 mg (n = 12), and 30 mg (n = 11) to patients with mild to moderate hypertension. Serial blood samples were obtained from 0 to 24 hours and from 0 to 48 hours after nisoldipine administration on days 1 and 7, respectively. Nisoldipine plasma concentrations were determined by gas chromatography with electron capture detection. No statistically significant difference was found in dose-normalized area under the curve between the four groups. Area under the curve (standardized to body weight) correlated to dose (r = .74, P less than .05). No significant difference existed in oral clearance (L/h/kg) when analyzed for equivalence across the four doses: 8.21 +/- 3.47 (5 mg), 11.84 +/- 13.85 (10 mg), 11.48 +/- 7.49 (20 mg), and 10.36 +/- 5.49 (30 mg). The present investigation characterizes the pharmacokinetics of nisoldipine core-coat tablets in hypertensive patients and demonstrates the dose proportionality or linearity of nisoldipine plasma concentrations and area under the curve, measured over a dose range of 5 to 30 mg.
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PMID:Multiple dose pharmacokinetics of four different doses of nisoldipine in hypertensive patients. 163 46

Nisoldipine is a calcium antagonist of the dihydropyridine group under investigation for treatment of hypertension. The authors have assessed the cardiovascular response to adrenergic stimulation by isometric exercise, cold pressor test and 70 degrees head-up tilt on four occasions: following placebo, acute and chronic administration of nisoldipine 5 mg or 10 mg o.d. in eighteen mild to moderately hypertensive patients (13 M, 5 F; age range 28-69 years). Blood pressure and heart rate were measured by automatic recorder. Blood pressure was significantly decreased at 2 h after administration of nisoldipine. Blood pressure maximal response at 3 min during isometric exercise following nisoldipine 10 mg chronic was significantly lower, compared to placebo as well as to a 5 mg dose (172/105 +/- 13/8 with 10 mg vs. 182/116 +/- 21/14 with 5 mg and 182/113 +/- 18/11 with placebo; p less than 0.05). Cardiovascular response to the cold pressor test showed a similar pattern; head-up tilt did not cause hypotension. The results of this study suggest that administration of nisoldipine in hypertensive patients slightly attenuates the pressor response to sympathetic stimulation by isometric exercise.
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PMID:Responses to sympathetic stimulation and tilting during antihypertensive treatment with nisoldipine. 182 33

Sequences of ventricular fibrillation-defibrillation cause transient hypertension; we hypothesized that this "adrenergic overshoot" might be blunted by the functional antiadrenergic effect of the calcium channel blocking drug nisoldipine, with a potentially beneficial reduction in myocardial oxygen requirements. However, other calcium channel blocking drugs have been shown to reduce shock success for defibrillation, a deleterious effect. Thus the purposes of this study were to assess the effect of nisoldipine on the hemodynamic responses to the sequences of ventricular fibrillation-defibrillation, and its effect on the energy requirements for defibrillation. In 16 dogs we administered intravenous nisoldipine (1 microgram/kg bolus followed by an infusion of 0.075 to 0.50 microgram/kg/min) to lower mean blood pressure 10% and 20% below baseline. Ventricular fibrillation was induced electrically, and shocks of varying energy levels (30, 50, and 100 joules) were administered to determine defibrillation energy requirements. Heart rates and blood pressures were recorded up to 3 minutes after each shock to determine hemodynamic responses. Measurements were made before nisoldipine administration and again at the two levels of drug-induced blood pressure decline. We found that the usual systolic blood pressure "overshoot" after defibrillation (typically maximum at 15 to 30 seconds after shocks) was significantly blunted after nisoldipine administration (p less than 0.05). Heart rate slowing after defibrillation (a cholinergic response) was not affected. Nisoldipine did not alter shock success rates, which varied from 12 +/- 7%SE at 30 joules to 68 +/- 12% at 100 joules. Thus nisoldipine blunted the "adrenergic overshoot" of systolic blood pressure following defibrillation, a potentially beneficial effect, without altering the energy requirements for transthoracic defibrillation.
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PMID:Effect of nisoldipine on hemodynamic responses to defibrillation. 200 Jul 51

We have studied the effects of nisoldipine, a new calcium channel antagonist, on the renin-angiotensin-aldosterone system and on plasma catecholamines in 10 healthy volunteers and in 29 patients with primary essential hypertension. Of these 29 patients, thirteen had normal renin hypertension (NRH), and sixteen had low renin hypertension (LRH). Eight healthy volunteers received placebo. Short-term (24 h) effects were measured in all subjects and long-term (up to 6 months) effects of 10-40 mg nisoldipine daily were monitored in the 29 hypertensive patients. Plasma renin activity (PRA) increased slightly, although this rise was not statistically significant, 1 h after the first dose of nisoldipine in both normotensive subjects and hypertensive patients. After 2 h PRA had returned to the pre-treatment level. No change in PRA was observed after administration of placebo. Plasma angiotensin II (AII) levels showed considerable variation after nisoldipine administration. Plasma aldosterone levels decreased despite the increase in PRA and AII concentrations. However, no concomitant reduction in urinary aldosterone excretion was observed. Plasma noradrenaline levels increased slightly 2-4 h after administration of nisoldipine, and decreased again thereafter, but no changes in plasma adrenaline levels were seen. Nisoldipine had no long-term effects on the renin-angiotensin-aldosterone system or on serum catecholamine levels.
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PMID:Nisoldipine--effects on the renin-angiotensin-aldosterone system and catecholamines. Studies in normotensive and hypertensive subjects. 225 22

The effects of the calcium antagonist nisoldipine on contractions stimulated by phenylephrine and B-HT 920 (agonists of alpha 1- and alpha 2-adrenoceptors) in isolated aortic rings from stroke-prone spontaneously hypertensive rats (SHRSP) and from normotensive Wistar-Kyoto rats (WKY) were investigated in vitro. Phenylephrine and B-HT 920 produced concentration-dependent contractions of vessels from both groups of animals. The absolute force of the contractions was less in the aortae from hypertensive rats after all doses of both agonists. Nisoldipine inhibited the B-HT 920-induced contraction much more in vessels from SHRSP than in those from normotensive WKY rats (IC50 = 1.5 X 10(-10) versus 7 X 10(-9) g/ml). The phenylephrine contractions were inhibited in SHRSP aortae by higher concentrations (IC50 = 8.5 X 10(-8) g/ml) of nisoldipine; in WKY, nisoldipine only produced a slight inhibition of phenylephrine-induced contractions. The inhibitory concentrations of nisoldipine on BHT-920-induced contractions are similar to those for the inhibition of the calcium or depolarization-induced contractions in other experiments. The alpha 2-agonist-induced contractions of rat aorta are dependent on transmembrane calcium supply. The higher efficacy of nisoldipine in aortae from SHRSP suggests an increased transmembrane availability of calcium ions in hypertension.
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PMID:Interference of the calcium antagonist nisoldipine with the abnormal response of vessels from hypertensive rats to alpha-adrenergic stimulation. 241 97

The haemodynamic effects associated with the onset of hypertension induced by infusion of adrenocorticotrophin (ACTH) were investigated in sheep. Analysis of haemodynamic data collected over 24 h by a computer-based monitoring system revealed that mean arterial pressure (MAP) was significantly increased after 4 h. Cardiac output was significantly raised after 1 h. The increased cardiac output was initially offset by a fall in calculated total peripheral resistance (CTPR) and MAP did not begin to rise until CTPR had returned to control values. This suggested that the return of CTPR to control values was essential for the development of hypertension. The development of ACTH-induced hypertension was prevented by both nisoldipine, a calcium channel blocker, and minoxidil, a vascular smooth muscle relaxant. Nisoldipine administration was also found to reverse established ACTH hypertension. A greater fall in MAP and CTPR occurred in the onset and established phase of ACTH hypertension sheep compared with normotensive controls. These results indicate that constriction of the peripheral vasculature is essential for the onset and maintenance of ACTH-induced hypertension in the sheep, and that the vasoconstriction does not involve a specific Ca21+-dependent mechanism because minoxidil was as effective as nisoldipine in abolishing the pressor response to ACTH. The onset of ACTH-induced hypertension in sheep is characterized by very rapid haemodynamic changes with an increase in cardiac output and a relative increase in CTPR after an initial peripheral vasodilatation.
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PMID:Rapid haemodynamic response to adrenocorticotrophin and the role of peripheral resistance in adrenocorticotrophin-induced hypertension in conscious sheep. 254

Nisoldipine is an orally administered calcium entry blocking drug structurally related to nifedipine. In limited clinical trials it has been shown to be effective and relatively well tolerated in the treatment of patients with chronic stable angina pectoris and mild to moderate essential hypertension. As for all dihydropyridine-calcium antagonists, its major properties include potent peripheral and coronary vasodilation and improvement in myocardial oxygen supply relative to demand. These actions occur without depression of cardiac conduction or left ventricular function. Short term clinical trials have shown nisoldipine to produce both symptomatic and objective improvements in patients with chronic angina of effort and have suggested a benefit in vasospastic angina. A small number of comparative trials indicate that nisoldipine is equally as effective as nifedipine. In addition, in combination with beta-adrenoceptor blockade nisoldipine appears to offer additional benefit compared with beta-blockade alone and is well tolerated. In patients with mild to moderate essential hypertension nisoldipine monotherapy, in 1 or 2 daily doses, has maintained blood pressure control and has also been a useful addition to diuretics and beta-adrenoceptor blocking drugs in patients with poorly controlled disease. Side effects appear to be dose related, generally mild and transient, and are primarily those resulting from potent peripheral vasodilation - headache, flushing and pretibial or ankle oedema. Although studies to date are promising, there are no published long term studies (greater than 1 year) of nisoldipine in comparison with other calcium entry blockers and other drugs currently in clinical use for the treatment of angina pectoris or hypertension. Until such studies are completed the exact place of nisoldipine in the treatment of these diseases remains to be established.
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PMID:Nisoldipine. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the treatment of angina pectoris, hypertension and related cardiovascular disorders. 306 58

Antihypertensive efficacy and tolerability of the dihydropyridine calcium antagonist nisoldipine were examined in a double-blind, placebo-controlled study. Twenty patients with hypertension (greater than 140/95 mmHg) uncontrolled by bendrofluazide plus atenolol were randomly allocated to receive nisoldipine, 10-20 mg daily, or placebo for six weeks. Nisoldipine, compared with placebo, lowered blood pressure (BP) by 31/21 mmHg (P less than 0.02/P less than 0.002) after two weeks. Thereafter its antihypertensive effect declined to 20/9 mmHg (NS/NS) at four weeks and 8/3 mmHg at six weeks (NS/NS). Compared with placebo, the rise in BP with nisoldipine during the last four weeks of the trial was highly significant (P less than 0.005). During this period BP rose by 14/11 mmHg (P less than 0.05/P less than 0.02) in the nisoldipine group so the apparent loss of effect was not attributable to a fall of BP in the placebo group. Compliance, as assessed by tablet counts, was satisfactory and nisoldipine treatment did not cause significant weight gain. The drug was not well tolerated and three patients withdrew from treatment because of side-effects. Tolerance to the antihypertensive effect of nisoldipine appears to develop rapidly and further studies should be performed to confirm this, and evaluate the mechanism.
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PMID:Rapid development of tolerance to the antihypertensive effect of nisoldipine. 306 6


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