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

The responses to a supine rest, norepinephrine (NE) and angiotensin II (Ang II) were investigated in the absence and presence of calcium antagonist nifedipine or diltiazem in essential (genetic, arterial) hypertension and normotension in humans. A supine rest significantly decreased blood pressure (BP), heart rate (HR), stroke volume index (SI), and cardiac output index (CI). On the contrary, the rest increased total peripheral vascular resistance index (TPRI) in both normotensives and hypertensives. The decrease in BP was significantly greater in hypertensives than in normotensives. NE significantly increased BP and TPRI, whereas it decreased HR, SI, and CI. The increase in BP was greater in hypertensives than in normotensives. Nifedipine and diltiazem inhibited the NE-induced increases in BP and TPRI. Ang II increased BP and TPRI, but it decreased HR, SI, and CI. Diltiazem did not inhibit the Ang-II-induced increases in both BP and TPRI. The increased responses to a rest and NE were observed in the early stage of essential hypertension. The increased responses may contribute to both the increase in BP and the induction of high blood pressure in essential hypertension. The calcium antagonists inhibited the NE-induced increases in BP and TPR. The results suggest that the antagonists inhibit the NE-dependent calcium influx and calcium release in the arterial smooth muscle. The observed responses to Ang II suggest that the antagonists may not inhibit Ang-II-dependent calcium-channel activity in the smooth muscle.
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PMID:Increased cardiovascular responses to norepinephrine and calcium antagonists in essential hypertension compared with normotension in humans. 241 85

This study was undertaken to evaluate the potential role of a perioperative calcium-channel blocker (Diltiazem) infusion in improving myocardial preservation. Forty consecutive CAD patients were randomly assigned to a control (C; n = 20) and a treated (D; n = 20) group. In patients in the latter group diltiazem was continuously infused at 0.5 to 2.0 mcg/kg/min i.v. from anesthesia induction until the aortic cross-clamping, and from myocardial reperfusion till the 48th postoperative hour. During the preCPB phase hypertension occurred less frequently in group D (3 vs 12 cases, p = 0.0033). In the immediate postischemic period, depression of contractility and the need for inotropic support were observed in 3 cases in group D and in 9 in group C (p = 0.0384). Postoperatively, group D patients had a lower incidence rate of hyperkinetic arrhythmias or conduction disturbances (p = 0.0218), as well as of ECG signs of ischemia (p = 0.0016). Significant CK enzyme level increase was noted in 13 patients in group C versus 4 in group D (p = 0.0040). Two perioperative myocardial infarctions were diagnosed, both in group C. These clinical data show that continuous perioperative infusion of diltiazem can effectively increase myocardial preservation during ischemic arrest, without unfavorable effects on the hemodynamics, electrical activity or mechanical performance of the heart.
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PMID:Myocardial protection by perioperative diltiazem drip: a clinical evaluation. 242 30

The effects of the calcium antagonist diltiazem on diastolic blood pressure and various parameters of erythrocyte membrane cation transport were evaluated in hypertensive patients with diastolic blood pressure between 95 and 110 mm Hg in a placebo-controlled, double-blind parallel study. Twenty-one patients completed the study; 13 received placebo, while 8 received diltiazem. Diastolic blood pressure, intracellular sodium and calcium concentrations, ouabain-sensitive Na+,K+-adenosine triphosphatase (ATPase) activity, and net sodium efflux and potassium influx across red blood cell membranes were examined in both groups at the end of placebo run-in, at the end of the titration phase, and at the completion of study. In the placebo group, none of the parameters changed significantly. In the drug-treated group, diastolic blood pressure declined by approximately 10% (placebo, 95.1 +/- 8.9; drug-treated, 86.9 +/- 4.9 mm Hg; p less than 0.03) at the end of the study. There were also reductions in intracellular sodium (placebo, 7.9 +/- 1.8; drug-treated, 5.2 +/- 0.4 mmol/L cells; p less than 0.002) and calcium (placebo, 13.5 +/- 1.6; drug-treated 10.8 +/- 3.3 mumol/L cells; p less than 0.03) concentrations, accompanied by a simultaneous rise in the activity of the ouabain-sensitive Na+,K+-ATPase of erythrocyte membranes (placebo, 7.1 +/- 1.1 X 10(-2); drug-treated, 9.0 +/- 0.6 X 10(-2) microM inorganic phosphate/hr/mg; p less than 0.001) at the end of the study. However, no significant change in the ouabain-insensitive moiety of the ATPase pump was found. Diltiazem treatment increased net sodium efflux and potassium influx.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Jan
PMID:Effects of diltiazem on cation transport across erythrocyte membranes of hypertensive humans. 243 9

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

To determine if oxygen-derived free radicals are mediators of endothelium-dependent contractions to acetylcholine in the aorta of spontaneously hypertensive rats (SHR), the mechanism of contraction to xanthine plus xanthine oxidase was studied. Rings, with and without endothelium, of thoracic aorta from normotensive Wistar-Kyoto (WKY) rats and SHR were suspended in organ chambers for isometric tension recording. Oxygen-derived free radicals caused concentration-dependent contractions; these contractions were twice as large in the aortas of SHR than in WKY rats. Deferoxamine reversed the response to xanthine oxidase to a small relaxation. Either allopurinol, superoxide dismutase, or catalase, or the combination of superoxide dismutase plus catalase reduced the contractions. Diltiazem inhibited the response to xanthine oxidase; in contrast, phentolamine plus propranolol did not affect it. Indomethacin and meclofenamate, but not tranylcypromine or dazoxiben blocked the contractions. Endothelium-dependent contractions to acetylcholine in aortas from the SHR were not affected by deferoxamine or superoxide dismutase plus catalase. These data suggest that hydroxyl radicals cause contractions in the rat aorta, which are dependent on extracellular calcium and mediated by activation of the cyclooxygenase in the vascular smooth muscle. The augmented contractions in the hypertensive strain are due to an increased reactivity of the smooth muscle to oxygen-derived free radicals. However, the lack of effect of the scavengers on endothelium-dependent contractions to acetylcholine suggests that the endothelium-derived contracting factor is chemically different from oxygen-derived free radicals.
Hypertension 1989 Jun
PMID:Contractions to oxygen-derived free radicals are augmented in aorta of the spontaneously hypertensive rat. 256 6

The most common interactions concern cardiovascular drugs. The combination of calcium antagonists (CA) and beta-blockers is more effective than single-agent therapy in stable effort angina and hypertension. But there is an increased risk of hemodynamic or electrophysiological side effects in patients with left ventricular or sinus dysfunction, or disturbances of conduction. Pharmacokinetic interactions have been observed in particular with verapamil (VE) which increases propranolol bioavailability. VE increases the T1/2 of elimination and plasma digoxin concentration following single or prolonged administration. The primary mechanism appears to be renal. These modifications increase the risk of digitalis intoxication. Diltiazem (DTZ) inconsistently increases steady state plasma digoxin levels. In healthy subjects, nifedipine (NF) increases plasma digoxin concentrations and decreases digoxin renal clearance. These findings have not been observed in patients with heart failure. NF therefore leads to less marked modifications in digitalis pharmacokinetics than do VE and DTZ. Nitrendipine and nicardipine interact only slightly with digoxin, and consequently there are no pharmacodynamic effects. In healthy subjects, VE increases quinidine t1/2 and markedly decreases its metabolic clearance. Conversely, quinidine increases plasma NF levels. The primary CA are extensively metabolized by liver microsome oxidases. These result in interactions with the drugs that are also metabolized by these enzymes, or able to modify their activity. VE and DTZ decrease antipyrine and carbamazepine clearance. VE, DTZ and nicardipine lead to a marked increase in plasma ciclosporin levels. Cimetidine, but not ranitidine, increases plasma NF levels. The effects on VE are controversial. Prolonged rifampicin treatment decreases plasma VE levels.
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PMID:[Drug interactions with calcium inhibitors in man]. 257 Nov 95

We studied 14 patients to determine whether sustained-release diltiazem is a satisfactory long-term substitute for the combination of propranolol plus hydrochlorothiazide (HCTZ), control phase, in the treatment of systemic hypertension with coexisting chronic stable angina pectoris. All patients had either one- or two-vessel coronary disease and normal left ventricular systolic function. Measurements were made during the control phase and 4 and 8 weeks after substitution of sustained-release diltiazem. Only the sitting blood pressure was available before the control phase (pretreatment). Blood pressure and heart rate were measured with patients supine, sitting, and 5 minutes after standing. Cardiac output was measured in the supine position using a computerized Doppler system, and stroke volume, mean arterial pressure, and total systemic resistance were calculated. Symptom-limited modified Bruce protocol treadmill tests were performed to determine time to onset of 1 mm ST segment depression, time to termination of exercise, reason for cessation of exercise, and maximum rate-pressure product. The patients were initially receiving 160-240 mg/day of propranolol (40-60 mg q.i.d.) plus 25-50 mg/day of HCTZ and, subsequently, 12 of 14 had substitution with 240 mg/day (120 mg b.i.d.) of sustained-release diltiazem, and two received 360 mg/day with one of these patients also receiving 50 mg/day of HCTZ. These patients are a subset of a larger group of patients in whom the response of blood pressure alone has been previously reported. Diltiazem resulted in reduction of blood pressure equivalent to that with the propranolol plus HCTZ combination.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of blood pressure, cardiac output, peripheral resistance, and exercise performance to substitution of calcium blocker for beta-blocker plus thiazide diuretic therapy in patients with both systemic hypertension and mild stable angina. 257 40

It is still uncertain whether antihypertensive therapy with calcium antagonists in general, and diltiazem in particular, can reduce left ventricular (LV) mass index and improve LV diastolic filling in hypertension. Therefore, 24 patients with mild to moderate hypertension (diastolic blood pressure 95 to 114 mm Hg before therapy) were randomly assigned to receive either a sustained-release preparation of diltiazem (n = 13) or placebo (n = 11) for 16 weeks in a double-blind, parallel-group protocol. M-mode and pulsed Doppler echocardiograms were performed at baseline and at the end of monotherapy. Echocardiograms were read blindly by 2 independent observers. The patients who received placebo exhibited no change in blood pressure, cardiac dimensions or LV function. Diltiazem significantly reduced both systolic pressure (151 +/- 14 to 139 +/- 12 mm Hg) and diastolic pressure (101 +/- 4 to 90 +/- 7 mm Hg, both p less than 0.05). Posterior wall and septal wall thicknesses decreased, but the changes were not statistically significant. End-diastolic dimension was reduced by diltiazem from 53 +/- 5 to 51 +/- 5 mm (p less than 0.05). LV mass index decreased significantly with diltiazem by 10%, from 125 +/- 21 to 113 +/- 23 g/m2 (p less than 0.05). The LV wall thickness to radius ratio remained unchanged during both diltiazem and placebo treatments. Changes in LV mass index and blood pressure did not correlate, suggesting that this response is influenced by factors other than pressure reduction alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of diltiazem on left ventricular mass and diastolic filling in mild to moderate hypertension. 252 55

A new class of antihypertensive agents has emerged for clinical consideration in the initial treatment of hypertension. These calcium antagonists are rapidly absorbed and reduce arterial pressure very promptly by antagonizing the pathophysiologic hallmark of the disease: an increased vascular resistance. Moreover, in reducing arterial pressure by means of arteriolar dilation, these agents do so without expanding intravascular volume and without inordinately stimulating the heart through reflex mechanisms. Vascular resistance is reduced in each of the major target organs of the disease: the heart, brain, and kidney. Reduction of coronary vascular resistance should be of particular value in patients with increased myocardial oxygen demands (e.g., with coronary arterial disease or with ventricular hypertrophy). Reduction of renal vascular resistance should be especially valuable for patients with renal functional impairment as a result of hypertensive vascular disease or with associated renal parenchymal diseases. In this respect, these agents reduce renal vascular resistance while maintaining glomerular filtration rate and reducing renal filtration fraction; these changes should reduce glomerular hyperfiltration and may inhibit promotion of glomerulosclerosis. Diltiazem may be of particular value because it may produce these effects while increasing renal blood flow. Clearly these agents reverse cerebral constriction and might be expected to improve blood flow to the brain; however, further study is anticipated and necessary.
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PMID:Calcium antagonists for initial therapy of hypertension. 266 85

The antihypertensive efficacy and frequency of adverse reactions following administration of diltiazem in a new slow-release formulation were compared with placebo in 34 patients with mild to moderate essential hypertension in a randomized, double-blind, crossover study. After 6 weeks of treatment with diltiazem (240 or 360 mg/day), average supine blood pressure (BP) decreased from 165 +/- 21/101 +/- 5 mm Hg at baseline to 152 +/- 16/93 +/- 4 mm Hg compared with 160 +/- 19/100 +/- 7 mm Hg with placebo (p less than 0.01/p less than 0.001). Standing BP decreased from 162 +/- 20/107 +/- 6 mm Hg at baseline to 150 +/- 14/101 +/- 5 mm Hg compared to 159 +/- 18/107 +/- 8 mm Hg with placebo (p less than 0.01/p less than 0.001). The supine heart rate after diltiazem was 65 +/- 7 beats/min and after placebo 69 +/- 9 beats/min (p less than 0.01). There were no hematologic side effects. Only minor differences between diltiazem and placebo were observed in some of the biochemical laboratory values. Four patients were withdrawn due to side effects during treatment with diltiazem and 2 with placebo. Diltiazem in a slow-release formulation given twice a day lowered blood pressure significantly as monotherapy in patients with mild to moderate hypertension and was well tolerated.
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PMID:Antihypertensive effect of diltiazem in a slow-release formulation for mild to moderate essential hypertension. 271 92


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