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)

Twenty-one patients with acute myocardial infarction were treated 7.6 +/- 4.9 h after the onset of symptoms with intravenous nifedipine for 48-72 h. No other vasoactive medication was given. Three patients with hypertension did not respond to nifedipine and were excluded from the analysis. In the remaining 18 patients, arterial blood pressure decreased significantly, whereas the heart rate remained unchanged. The mean pulmonary artery and capillary pressure showed a slight but significant decrease. Cardiac index increased significantly. In nine patients, two-dimensional and M-mode echocardiography could be analyzed. The left ventricular ejection fraction increased significantly from 50 +/- 3% to 56 +/- 1%. There was a significant decrease in systemic peripheral resistance index, systolic wall stress, and the calculated myocardial oxygen consumption. These hemodynamic effects persisted throughout the study period. The therapy was well controllable, and there were no significant side effects. Nifedipine improves left ventricular function without an increase in myocardial oxygen demand. This effect is primarily due to afterload reduction.
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PMID:Effect of intravenous nifedipine on hemodynamics and left ventricular function in acute myocardial infarction. 248 22

Nifedipine reduces blood pressure predominantly by reducing systemic vascular resistance due to a direct vasodilating action on the arterioles. This peripheral vasodilation appears greater the more severe the hypertension. Nifedipine also causes a long-term loss of sodium, which may be an additive mechanism for the blood pressure fall. In patients who are not controlled on nifedipine alone, studies have demonstrated an additive effect of beta blockers and converting-enzyme inhibitors on blood pressure. There is controversy about whether diuretics have an additive effect on blood pressure in patients already on nifedipine.
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PMID:Nifedipine and hypertension: roles of vasodilation and sodium balance. 248 1

A 46 year old woman with hypertension and left ventricular hypertrophy accompanied by an atrial septal defect is reported. Hemodynamic changes induced by balloon occlusion and concomitant nifedipine were studied. Left ventricular failure appeared after balloon closure of the defect. Nifedipine decreased the increment in left ventricular end-diastolic pressure induced by balloon occlusion. After the reduction of systemic vascular resistance, the ratio of intracardiac shunt flow was still larger. Surgical closure of the defect was performed and the postoperative course was good with the use of vasodilators.
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PMID:A case of atrial septal defect combined with hypertension and left ventricular hypertrophy. Left ventricular failure induced by balloon occlusion and the effect of nifedipine. 252 9

As many as 32 patients with moderate arterial hypertension were examined. According to unidimensional echocardiography, the improvement of early diastolic filling of the hypertrophied left ventricle of the heart was recorded during 4 weeks of the treatment with nifedipine, a dihydropyridine blocker of calcium channels. The favourable effect on diastolic filling function was combined with an efficient control over arterial pressure which was determined by a decrease in the systemic vascular resistance. Nifedipine did not produce any depression of contractile and pump functions of the heart.
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PMID:[Nifedipine in the treatment of hypertension. An echocardiographic assessment of the hemodynamic effects]. 253 75

Numerous epidemiological studies have shown that systolic and systodisystolic hypertension constitute major risk factors for damaging or fatal cardiovascular accidents in the elderly as well as the young. Furthermore reducing the blood pressure also reduces the risk. In 1983 Fleckenstein investigated the Ca++ and MG++ contact of human arteries and clearly demonstrated that titres of both but especially Ca++ in the arterial wall increased progressively with age. The Authors themselves caused calcinosis of the arterial wall in rats treated with Vitamin D3 and Dihydrotachysterol and were able to prevent the occurrence with Verapamil. It is against this background that the present study compared the efficacy and tolerability of two anti-hypertensive drug groups in the calcium antagonists and the ACE inhibitors (Enalapril Maleate) used individually on two groups of elderly hypertensives. A group of 123 out patients with a mean age of 73 and all suffering from slight-to-moderate hypertension were monitored for 6 months being subjected to the following examinations: clinical assessment including blood pressure measurements lying and standing, biohumoral tests, remote heart X-rays, echocardiography (to establish the Reichek systolic wall stress index) and ECG. The clinical examination and ECG were repeated every 2 weeks for the first 6 months and once a month thereafter. The heart X-rays, echocardiogram and biohumeral tests were performed every 6 months. The patients were divided into two groups I and II and assigned to the selected treatment. The Group I patients were then divided into 3 subgroups and treated with 3 different calcium antagonists (Nifedipine R; Verapamil R and Diltiazem). All group II patients were treated with Enalapril Maleate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Calcium antagonists vs ACE inhibitors in the treatment of essential arterial hypertension in the aged]. 254 2

Nifedipine is an effective agent in hypertensive emergencies as well as in the long-term management of hypertension especially for the patients with an increased risk of cerebral hypoperfusion. Nifedipine exerts its blood lowering effect by reducing total peripheral resistance including cerebrovascular resistance. Despite the marked reduction of perfusion pressure, the cerebral blood flow is maintained by nifedipine.
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PMID:[The action of fenigidin (nifedipine) on central hemodynamics and cerebral blood flow in hypertension]. 255 33

We have studied the contribution of neurohumoral and structural factors to pressor responsiveness and peripheral resistance in mild/moderate hypertension. Pressor responses to intravenous infusions of phenylephrine (an alpha1 agonist) and angiotensin II were studied in groups of patients with essential hypertension before and after treatment, for 6 weeks with either nifedipine (20 mg bid), enalapril (20 mg daily) or doxazosin (2 mg daily). All drugs lowered blood pressure to a similar extent. Pressor responsiveness to both phenylephrine and angiotensin II showed wide intersubject variation when expressed as the dose of agonist required to raise mean arterial pressure by 20 mmHg (PD20). A group of age-matched normotensive controls showed a similar PD20 for phenylephrine to hypertensives. Angiotensin 11 sensitivity was greater in hypertensives. Drug treatment had different effects in hypertensive patients. Doxazosin, an alpha blocker, reduced the responsiveness to phenylephrine but had no effect on responses to angiotensin II. Nifedipine attenuated responses to both agonists while treatment with enalapril increased responsiveness to both phenylephrine and angiotensin II. We have not found evidence of systematic differences in alpha 1 receptor responses in hypertensives and different "vasodilator" drugs can lower blood pressure with widely different effects on adrenergic and non-adrenergic vascular responses.
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PMID:Pressor responsiveness in essential hypertension and the effects of treatment with an alpha blocker, calcium antagonist or ACE inhibitor. 256

Nifedipine reduces blood pressure predominantly by reducing systemic vascular resistance due to a direct vasodilating action on the arterioles. This peripheral vasodilation appears greater the more severe the hypertension. Studies have demonstrated an additive effect of beta blockers and converting-enzyme inhibitors in patients not controlled with nifedipine alone. Although there is a controversy about whether diuretics have an additive effect on blood pressure in patients already taking nifedipine, it would appear that the blood pressure-lowering effect of thiazide is blunted. Studies have shown that a high sodium intake may enhance the acute blood pressure-lowering effect of nifedipine. Nifedipine does cause a long-term reduction in sodium balance.
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PMID:Nifedipine and systemic hypertension. 257 Dec 89

We assessed the effect on blood pressure of administration of slow-release nifedipine tablets (20 mg) by continuous intraarterial blood pressure monitoring (Oxford system) in 10 patients with untreated essential hypertension. Blood pressure was recorded under control conditions and during nifedipine therapy. During each monitoring period patients were instructed to perform various types of exercise. The initial dose of nifedipine was 20 mg twice a day (8:00 a.m. and 8:00 p.m.). For patients in whom arterial pressure control was not achieved, the dose of the drug was increased at weekly intervals, first to 40 mg in the morning and 20 mg at night and then to 40 mg twice a day. The average daily dose was 52 mg. Nifedipine twice a day significantly reduced systolic and diastolic blood pressures both during the day and during the night. The rise in blood pressure due to dynamic or isometric exercise or to mental testing was blunted. Heart rate did not change. Orthostatic hypotension was not observed, and there were only minor side effects, which did not require withdrawal of the patient from the trial. Bioavailability of nifedipine from this preparation was satisfactory, as shown by plasma concentrations which remained constantly in the therapeutic range. Thus, slow-release nifedipine given twice a day represents an effective treatment in patients with essential arterial hypertension. The reduced frequency of administration required may improve patient compliance with this treatment.
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PMID:Evaluation of the efficacy of slow-release nifedipine in systemic hypertension by ambulatory intraarterial blood pressure monitoring. 258 Jan 35

Because captopril alone does not control blood pressure in all patients with essential hypertension, studies were performed to assess the effect of sodium intake and of captopril combined with hydrochlorothiazide, propranolol, and nifedipine. Captopril given for 5 days to normotensive subjects having high, normal, and low sodium intakes reduced blood pressure the most in those on the lowest intake; the fall correlated with that in plasma angiotensin II. When 12 patients with moderate hypertension had hydrochlorothiazide added to captopril their blood pressure fell significantly. When propranolol was added to captopril, however, there was no further fall in blood pressure. When propranolol was added to captopril and a diuretic, pressures measured 4 and 6 h after the last dose of captopril showed reduced values compared with placebo; pressures measured 2 and 12 h after did not. Nifedipine added to captopril reduced blood pressure more than either drug alone. When renin and angiotensin are low, as they may be in essential hypertension, captopril is less effective; its effectiveness should increase if sodium is restricted. Both diuretics and nifedipine increase the effectiveness of captopril; propranolol does not, although it may prolong captopril's action. Experience in patients with resistant hypertension suggests that adding nifedipine to captopril may reduce the need for diuretics, while adding captopril to nifedipine may reduce the need for beta-blockers.
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PMID:Captopril: contrasting effects of adding hydrochlorothiazide, propranolol, or nifedipine. 258 Jan 82


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