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

Aortic rings isolated from normotensive Sprague-Dawley rats (CONT) exhibited spontaneous tone when the preparations were stretched. After administering deoxycorticosterone acetate (DOCA), the rats became hypertensive, and this spontaneous tone increased remarkably. The spontaneous tone was dependent on the extracellular calcium concentration. Incubation with the calcium entry blocker D-600 attenuated the spontaneous response to a greater degree in rings from DOCA rats than in rings from CONT rats. Nifedipine relaxed the already developed spontaneous tone. Removal of the endothelium greatly depressed spontaneous tone, but did not diminish the contraction caused by norepinephrine. On the basis of our findings, we conclude that 1) spontaneous tone depends on calcium influx, presumably through specific stretch-operated membrane channels, 2) these stretch-dependent channels are blocked by D-600 and nifedipine, 3) spontaneous tone is enhanced in DOCA hypertension, and 4) the endothelium appears to act as a receptor for stretch, mediating--at least in part--the spontaneous contractile response by releasing a constrictor agent.
Hypertension 1989 Mar
PMID:Endothelium-mediated spontaneous response in aortic rings of deoxycorticosterone acetate-hypertensive rats. 292 Oct 80

Nifedipine long acting tablets were substituted for converting enzyme inhibitors in eight patients with renovascular hypertension. A significant drop in blood pressure was observed. Nifedipine was shown to be as effective (in lowering blood pressure) as a drug that acts directly on the renin angiotensin system. These data offer support for previously reported findings that the action of angiotensin II is calcium mediated.
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PMID:Nifedipine as a substitute for converting enzyme inhibitors in the treatment of renovascular hypertension. 299 18

Nifedipine, in a slow release preparation, was given at a mean daily dosage of 47 +/- 4 mg to 12 patients with severe hypertension in whom arterial pressure was not satisfactorily controlled (mean blood pressure, 172 +/- 6/111 +/- 4 mmHg) by the association of a converting enzyme inhibitor and a diuretic. Nifedipine administration induced a marked decrease in blood pressure (to 133 +/- 3/85 +/- 3 mmHg), serum potassium and plasma aldosterone. Following adequate control of hypertension and because of severe hypokalaemia in some patients, the diuretic was discontinued in 10 subjects. After 1.7 +/- 0.5 months of treatment by the converting enzyme inhibitor and nifedipine, no change in arterial pressure occurred whilst serum potassium returned to normal in most patients. These results demonstrate that nifedipine may be useful in patients with residual elevation of arterial pressure when treated by converting enzyme inhibitor and diuretic. However, in such patients serum potassium level should be carefully monitored. In addition, our observations suggest that calcium blockers may be an effective alternative to diuretics in patients receiving a converting enzyme inhibitor.
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PMID:Effect of nifedipine in hypertension not controlled by converting enzyme inhibitor and diuretic. 302 71

The relaxation of phenylephrine-contracted blood vessels by acetylcholine, nitroprusside, or atrial natriuretic factor has been linked to elevations in cyclic guanosine 3',5'-monophosphate (cGMP). Also, 8-bromo-cGMP can induce vascular relaxation in isolated vascular smooth muscle contracted with phenylephrine. We determined whether these cGMP-dependent vasodilators could relax isolated rat aortas contracted with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate. cGMP was measured by radioimmunoassay. Acetylcholine, nitroprusside, and atrial natriuretic factor induced relaxation in vascular smooth muscle contracted by 12-O-tetradecanoylphorbol-13-acetate. These relaxation responses were accompanied by elevations of cGMP. However, the sensitivity to these vasodilators was markedly decreased in phorbol ester-contracted vessels compared to phenylephrine-contracted vessels. Nifedipine and superoxide dismutase induced small but significant relaxations in phorbol ester-contracted vessels; however, blood vessels contracted with phenylephrine and phorbol ester relaxed completely with papaverine. There was a marked decrease in sensitivity to 8-bromo-cGMP in phorbol ester-treated vessels compared to phenylephrine-contracted vessels. Contractions induced by phorbol ester were not inhibited by amiloride or chlorpromazine. Also, following incubation in potassium-free salt solution, vessels incubated with phenylephrine or phenylephrine and phorbol ester underwent similar relaxations when exposed to potassium chloride. The contractile state induced by phorbol ester has decreased sensitivity to cGMP-dependent vasodilators. This may be due to nonspecific effects of the phorbol ester or to the mechanism by which protein kinase C activation maintains vascular tone.
Hypertension 1987 Jun
PMID:Phorbol ester, vascular relaxation, and cyclic guanosine 3',5'-monophosphate. 303 7

A case is reported of bronchial stenosis due to a vascular cause in a patient with chronic obstructive lung disease, cor pulmonale and pulmonary arterial hypertension. This led to right lower lobe atelectasis and acute respiratory failure (pHa 7.24; PaCO2 85 mmHg; PaO2 44 mmHg) with important right-to-left shunting. This diagnosis was only suggested on day 7 by fibreoptic bronchoscopy and confirmed a week later by tomography and digital angiography. Nifedipine, used to reduce the pulmonary arterial hypertension, increased the cardiac index (31.min-1.m-2 to 3.3.1.min-1.m-2) and oxygen transport (488 ml.min-1.m-2 to 554 ml.min-1.m-2), despite increasing the shunt effect (Qs/QT: 26% to 31%). This and the antiinflammatory action of methylprednisolone were probably responsible for the favourable outcome.
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PMID:[Bronchial stenosis of vascular origin in pulmonary arterial hypertension]. 304 7

Both nifedipine and captopril are effective in the treatment of systemic hypertension in the elderly, but their effects on cardiac function in this age group have not been evaluated. We studied the effects of acute oral administration of 20 mg nifedipine and 12.5 mg captopril on systolic and diastolic cardiac function, as evaluated by a radionuclide method, in 14 elderly hypertensives, mean age 73.4 +/- 3.9 years. The radionuclide studies were performed 1 h after ingestion of nifedipine and 1.5 h after captopril, on separate days. Nifedipine accelerated the heart rate whereas captopril slowed it. Nifedipine increased the ejection fraction by 2.6 +/- 14.6% but captopril increased it by 13 +/- 15.3%. Nifedipine reduced the left ventricular peak ejection rate by 4.8 +/- 21.7% whereas captopril increased it by 18 +/- 24.3%. Nifedipine increased the peak filling rate by 14.3 +/- 41.6% and captopril increased it by 27.6 +/- 32.6%. Nifedipine reduced the time to peak filling rate by 24.9 +/- 27.0%, but captopril reduced it by 68.8 +/- 59.6%. All these differences were statistically significant. Therefore, captopril improves some diastolic and systolic parameters of cardiac function more than nifedipine does. Other parameters are impaired by nifedipine but improved by captopril.
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PMID:Comparative effects of captopril and nifedipine on diastolic and systolic cardiac function in elderly hypertensive patients. 306 82

The use of calcium antagonists and diuretics in combination for treatment of hypertension is controversial. In a single-blind study 16 patients (8 men, 8 women, age range 39 to 62 years) with primary hypertension of mild to moderate degree were given slow-release nifedipine 20 mg twice daily for 6 weeks, thereafter either chlorthalidone 25 mg (Group A) or placebo (group B) daily was randomly added for a further 6-week period. Blood pressure (BP), heart rate, plasma renin activity (PRA), aldosterone, and 24 hour urinary electrolytes were evaluated. Nifedipine decreased supine BP from 159/92 +/- 16/8 to 151/89 +/- 10/6 mmHg in group A and from 162/94 +/- 20/12 to 145/85 +/- 14/6 mmHg in group B. A further fall to 139/84 +/- 7/6 mmHg (p less than .05) was observed after addition of chlorthalidone. PRA significantly increased with combined treatment compared to baseline (3.3 +/- 0.8 to 9.9 +/- 3.3 ng/ml/hr; p less than 0.05). A slight reduction of 24-hour urinary calcium was observed after the addition of chlorthalidone. These data indicate that the combination of nifedipine and chlorthalidone might be beneficial in the treatment of arterial hypertension.
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PMID:Addition of chlorthalidone to slow-release nifedipine in the treatment of arterial hypertension: a controlled study versus placebo. 315 30

Nifedipine was used successfully in nine patients with refractory hypertension and left ventricular hypertrophy who had symptoms of congestive heart failure despite preserved left ventricular systolic function. The administration of 10 or 20 mg of nifedipine resulted in an acute decline in BP, from 211 +/- 8/105 +/- 6 mm Hg to 153 +/- 9/78 +/- 5 mm Hg. Six patients received nifedipine and one patient received long-term verapamil therapy (mean follow-up, 16 +/- 4 weeks). In addition to sustained BP control, signs and symptoms of congestive heart failure were greatly improved in all patients treated long term with calcium channel antagonists. No adverse reactions were reported, but a short duration of action limited their usefulness in some patients. Nifedipine seems to be particularly beneficial in this subgroup of severe hypertensive patients with heart failure presumably due to diastolic stiffness of the left ventricle.
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PMID:Nifedipine in severely hypertensive patients with congestive heart failure and preserved ventricular systolic function. 315 67

Dynamic and kinetic variability account for the large intersubject differences in the antihypertensive response to nifedipine, and a clear concentration-effect relationship has not been established. The effects of placebo, first dose, and chronic (1 and 6 weeks) treatment with nifedipine were studied in 14 subjects with essential hypertension using an integrated kinetic-dynamic model to calculate individual subject responsiveness in terms of fall in blood pressure per unit change in drug concentration. Nifedipine concentrations were well correlated with the fall in systolic blood pressure in individual subjects, and the mean responsiveness was -0.48 mm Hg/ng/ml after the first dose, -0.45 mm Hg/ng/ml after 1 week, and -0.49 mm Hg/ng/ml after 6 weeks. The responsiveness to the first dose of nifedipine was significantly correlated with the responsiveness after 1 (r = 0.83) and 6 weeks (r = 0.78) of therapy and with the height of the pretreatment blood pressure (r = 0.6). This study incorporated kinetic as well as dynamic information to characterize the antihypertensive response to nifedipine and identify nifedipine concentration-effect relationships in individual hypertensive subjects.
Hypertension 1988 Oct
PMID:Nifedipine: individual responses and concentration-effect relationships. 316 52

The short-term effect of the calcium channel blocker, nifedipine, on maternal hemodynamics and organ perfusion was investigated in 12 hypertensive term-pregnant, spontaneously hypertensive rats by means of the radioactive-labeled microsphere technique. The normal fall in blood pressure during pregnancy was prevented by reducing litter size to two conceptuses on day 7 of gestation. Nifedipine (200 micrograms/kg) effectively lowered mean arterial pressure 25% by decreasing total peripheral resistance 38%. Cardiac output was increased 15%. Blood flows to the splanchnic region and the reproductive organs were increased after nifedipine administration. The increase in blood flow to the reproductive organs was the result of increased ovarian and uterine wall perfusion caused by large reductions in vascular resistances. Placental blood flow was not significantly altered, but resistance was decreased. Thus, the use of nifedipine to lower maternal blood pressure in pregnancy complicated by extreme hypertension does not necessarily decrease uteroplacental perfusion.
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PMID:Nifedipine does not adversely affect uteroplacental blood flow in the hypertensive term-pregnant rat. 320 22


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