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

Approximately 60 million people in the United States have hypertension (BP greater than or equal to 140/90 mm Hg), 40 million have arthritis clinically suitable for nonsteroidal anti-inflammatory drug (NSAID) therapy, and millions take NSAIDs for nonarthritic conditions, creating considerable potential for concomitant administration of NSAIDs and antihypertensive agents. It is estimated that more than 20 million people are on concurrent therapy. Most NSAIDs produce mild elevations of normal blood pressure levels and can partially or completely antagonize the effects of many antihypertensive drugs. The effect on blood pressure can vary from no effect to hypertensive crisis. In pooled studies, the average increase in mean arterial pressure was 10 mm Hg, and duration was short-lived or chronic. Significant interactions occur in about 1% of patients per year. The risk is greatest in the elderly, blacks, and patients with low-renin hypertension. NSAIDs may block the antihypertensive effects of thiazide and loop diuretics, beta-adrenergic blockers, alpha-adrenergic blockers, and angiotensin-converting enzyme inhibitors. No interactions have been reported with centrally acting alpha agonists or the calcium channel blockers. The mechanism of the hypertensive effects of NSAIDs seem primarily related to their ability to block the cyclo-oxygenase pathway of arachidonic acid metabolism, with a resultant decrease in prostaglandin formation. The prostaglandins are important in normal modulation of renal and systemic vascular dilatation, glomerular filtration, tubular secretion of salt and water, adrenergic neurotransmission, and the renin-angiotensin-aldosterone system. Blockade of salutary effects of prostaglandins by NSAIDs results in a complex series of events culminating in attenuation of the effects of many antihypertensive agents. High-risk patients treated with NSAIDs should be identified and have blood pressure, renal function, and serum potassium frequently monitored.
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PMID:Nonsteroidal anti-inflammatory drugs and antihypertensives. 190 2

Calcium channel antagonists are commonly used to treat chronic hypertension. Several studies of intact vascular tissues suggest that these agents may impair the production of the endothelium-derived relaxing factor and alter endothelium-dependent vascular relaxation. These studies are difficult to interpret because the calcium channel antagonist may have direct effects on vascular smooth muscle. In our study, a chemiluminescence assay was used to measure the release of nitrogen oxides from bovine aortic endothelial cells (BAEC) grown in monolayer. Under basal conditions, the release of nitrogen oxides was 0.2 nmol/100 mg protein and was increased approximately two-fold by 0.1 micrograms, bradykinin. Incubations with diltiazem, verapamil, and nifedipine for 60 min did not influence the basal and bradykinin-stimulated release of nitrogen oxides by BAEC. These data illustrate that the production of the endothelium-derived relaxing factor is not altered by the calcium channel antagonist, and are compatible with an absence of L-type calcium channels in vascular endothelial cells. Chronic hypertension produces myriad adverse effects in the coronary circulation. After coronary occlusion, infarct size, expressed as a function of myocardial mass perfused, is increased by 33%, and the wavefront of infarction from subendocardium to subepicardium is hastened. Both chronic and acute hypertension produce numerous abnormalities of coronary flow regulation. These include impairments of autoregulation, changes in vascular responsiveness, and alterations of endothelial cell function. Many of these may worsen the clinical consequences of ischemic heart disease, either by producing structural alterations of the coronary vasculature, or equally importantly, by altering coronary vascular responsiveness to either mechanical or neurohumoral stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension and the coronary circulation. With special attention to endothelial regulation. 191 Jun 38

Physical exercise can increase urinary albumin excretion rate (UAER) in diabetic patients without microalbuminuria at rest (stage II diabetic nephropathy) or with baseline microalbuminuria (stage III diabetic nephropathy). The aim of this study was to compare the acute effects of captopril, an ACE inhibitor, and nifedipine, a calcium channel blocker, on exercise-induced microalbuminuria in hypertensive insulin-dependent (Type I) and non-insulin-dependent (Type II) diabetic patients with early stage nephropathy. Non-obese diabetic patients, 13 Type I (7 with stage II and 6 with stage III nephropathy) and 14 Type II (6 with stage II and 8 with stage III nephropathy), with hypertension, WHO stages I-II, underwent five submaximal cycloergometric tests: the first two in basal conditions, the other three after 24 hour administration of captopril (25 mg twice daily), placebo (1 tab twice daily) or nifedipine AR (20 mg twice daily) according to a randomised, double-blind design. Acute administration of both captopril and nifedipine was able to reduce exercise-induced microalbuminuria in hypertensive Type I and Type II diabetic patients regardless of the stage of their nephropathy. Captopril reduced systolic blood pressure less than nifedipine, in both Type I and Type II diabetics, but was more effective than nifedipine in blunting exercise-induced microalbuminuria, especially in Type I diabetics.
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PMID:Albuminuria induced by exercise in hypertensive type I and type II diabetic patients: a randomised, double-blind study on the effects of acute administration of captopril and nifedipine. 192 Mar 40

Post-renal transplant hypertension remains a common problem. The most frequent causes now are chronic rejection and cyclosporine-induced hypertension. Before the development of cyclosporine, renin-dependent hypertension was the dominant pathophysiological mechanism but now, with the widespread use of cyclosporine, a salt-dependent mechanism is the major one. In severe "inappropriate" hypertension, potentially surgically remediable causes such as renal artery stenosis of the allograft artery or renin release from the native kidneys should be considered. Cyclosporine causes hypertension in normal subjects and in all solid organ transplants. The most likely mechanism is renal vasoconstriction with subtle retention of sodium chloride together with systemic vasoconstriction. The vasoconstriction, as yet, is not associated with any specific vasoconstricting agent nor does there appear to be a specific antagonist. Indeed, increased sensitivity to many different vasoconstrictors has been demonstrated. The major site of vasoconstriction appears to be in the afferent arteriole, and optimum antihypertensive therapy is probably provided by calcium channel blockers if the hypertension is due to cyclosporine. Because post-renal transplant hypertension is often multifactorial in origin, however, it is not surprising that the use of combined antihypertensives is often necessary.
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PMID:Pathophysiology and treatment of posttransplant hypertension. 193 42

Nifedipine, a calcium channel blocker, is widely used in the management of hypertension, angina and cardiac arrhythmias. In this study, the bioequivalence of two pharmaceutical formulations of nifedipine, Nifecard (10 mg capsules) manufactured by Dar Al-Dawa Development and Investment Co, Ltd. and Adalat (10 mg capsules) manufactured by Bayer Pharmaceutical Company, was assessed in twelve healthy male subjects. Nifecard or Adalat was given orally on two occasions separated by one week wash-out interval. Blood samples for the determination of plasma nifedipine concentration were taken for 8 hours following drug administration. Blood pressure and pulse were also measured after each treatment. Plasma nifedipine concentrations were measured by a simple, sensitive and reproducible HPLC method. There were no significant differences in oral absorption, Cmax, tmax, t1/2 and AUC between Nifecard and Adalat. Also, Nifecard and Adalat produced similar hemodynamic profiles (blood pressure and pulse). In conclusion, our results demonstrate that both Adalat and Nifecard are bioequivalent and produced similar pharmacological effects.
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PMID:Pharmacokinetics and pharmacodynamics of two commercial oral nifedipine products. 193 93

Hypertension and diabetes mellitus are both common conditions which frequently co-exist. The calcium channel blockers are potentially diabetogenic since insulin secretion may be impaired by their use. The aim of this study was to determine whether nitrendipine, a second generation dihydropyridine derivative calcium antagonist, is capable of interfering with carbohydrate metabolism and insulin secretion in hypertensive diabetics at the doses commonly used in therapy. In a 12-week double blind placebo-controlled randomized clinical trial, the effects of nitrendipine (20 mg/day) on arterial blood pressure, glycaemic homeostasis and other metabolic parameters were evaluated in 30 patients with mild to moderate essential hypertension and type II diabetes mellitus. The results showed nitrendipine to be an effective antihypertensive agent which neither impaired the overall glucose homeostasis nor caused any other potentially harmful metabolic side effect. In conclusion, these data suggest that the calcium channel antagonist nitrendipine is a metabolically safe drug to use in the treatment of hypertension, especially in patients with diabetes mellitus.
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PMID:[Antihypertensive efficacy of nitrendipine and its effects on carbohydrate metabolism. A controlled clinical study versus placebo]. 194 44

The major differences that have been recognized between black and white hypertensives are primarily epidemiologic, with hypertension being more prevalent, having an earlier onset, and having more severe sequelae in the black population. The cause of the problem in both black and white people remains obscure, but it appears that a difference in sodium handling may contribute to the particular hemodynamic and hormonal profile of black hypertensives. Salt sensitivity, expanded plasma volume and low renin levels have been the hallmark of the black hypertensive. Complications such as stroke and left ventricular hypertrophy remain the major sequelae of this disease in blacks. Finally, a current study confirmed the improved efficacy of antihypertensive therapy in blacks to diuretics and calcium channel blockers and a somewhat lower efficacy profile to angiotensin converting enzyme inhibitors and beta blockers, although the latter classes of agents have shown better response in blacks than previously thought.
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PMID:Hypertension in blacks. 194 90

The effects of antihypertensive drugs, such as nifedipine, chlorpromazine, reserpine and thiopental on mean arterial blood pressure (ABP), mean intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were studied in 43 patients with systemic hypertension and intracranial hypertension due to hemorrhagic cerebrovascular diseases and other causes. These drugs are commonly used in neurosurgical practice for the treatment of systemic hypertension. Nifedipine, chlorpromazine and reserpine reduced the mean ABP, raised the mean ICP and decreased the CPP. The effects of these drugs on mean ICP and CPP were more pronounced in patients with severely increased ICP (more than 40 mmHg) than in patients with moderately increased ICP (20-40 mmHg). Thiopental reduced both mean ABP and ICP, whereas the CPP was unchanged from the preadministration level. During thiopental administration, however, respiratory depression was observed, and hence, intubation and ventilation were required. We suggest that, in the treatment of systemic hypertension in patients with increased ICP, barbiturates are more desirable than agents with calcium channel or alpha-adrenergic blocking actions, despite the problem of respiratory control.
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PMID:Effects of antihypertensive drugs on intracranial hypertension. 195 Feb 24

Treatment of hypertension in patients with NIDDM should be administered with special attention not to increase insulin resistance nor to impair insulin secretion capacity. The coexisting risk for coronary artery disease and myocardial infarction should not be increased by undesired drug effects on the plasma lipoprotein profile. Late lesions of diabetes mellitus (nephropathy, neuropathy) have also to be taken into account. Consequently angiotensin converting enzyme inhibitors, if necessary combined with calcium channel blockers, should be administered first. If blood pressure is thus not sufficiently controlled, alpha-adrenergic blockers, vasodilating agents or sympatholytics may be added. Once insulin treatment is installed, or if required for other reasons (nephropathy, congestive heart failure, cardiac arrhythmia), also diuretics and beta-adrenergic blockers are indicated in antihypertensive treatment of diabetic patients.
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PMID:[Hypertension in type II diabetes mellitus]. 195 Mar 78

The long-term effects of converting enzyme inhibitors and calcium channel blockers on proteinuria and the progression of renal disease in patients with hypertension and chronic renal insufficiency are not well established. We have studied the long-term effects of treating hypertension with an angiotensin-converting enzyme inhibitor, enalapril, and a calcium channel blocker, nicardipine, on urinary albumin excretion (UAE) and on renal function in 16 patients with hypertension and chronic renal insufficiency (creatinine clearance ranging between 17 and 62 ml/min). After 1 year of treatment, these agents caused a similar decrease in blood pressure. Only enalapril, however, caused a significant decrease in UAE (from 641 +/- 98 to 292 +/- 47 mg/24 h, p less than 0.01), whereas UAE did not change in the group treated with nicardipine (675 +/- 78 vs. 601 +/- 75 mg/24 h). Creatinine clearance at the beginning of the study was similar in the group treated with enalapril and in the group treated with nicardipine (35 +/- 3.6 vs. 40 +/- 4.1 ml/min). After 1 year of follow-up, creatinine clearance remained unchanged in both groups of patients. These studies demonstrate that both enalapril and nicardipine can effectively reduce blood pressure in patients with hypertension and chronic renal insufficiency. Enalapril but not nicardipine, however, appears to reduce urinary albumin excretion in these patients. Whether the reduction in UAE has any significant impact on the progression of renal disease remains to be established.
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PMID:Long-term effects of enalapril and nicardipine on urinary albumin excretion in patients with chronic renal insufficiency: a 1-year follow-up. 195 74


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