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

Calcium antagonists are potent arterial vasodilators with no long-term effect on sympathetic reflex activity or sodium and volume retention. This favourable haemodynamic profile makes them suitable for monotherapy of hypertension, where they act to reduce an enhanced, calcium-influx-dependent vasoconstrictor mechanism which may be brought about by altered smooth-muscle cation handling and increased intracellular concentrations of free calcium. Clinical studies have proved the efficacy, safety and acceptability of calcium antagonists alone or in combination with other drugs in uncomplicated hypertension; calcium antagonists are particularly effective in older patients, those with low renin levels and, possibly, black patients. These properties and the efficacy of calcium antagonists in the treatment of severe and accelerated hypertension or hypertensive emergencies make them a valuable addition to the drugs already available for the treatment of hypertension.
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PMID:Calcium antagonists in hypertension. 331 26

The effect of short-term diuretic treatment on the action of clonidine was evaluated in eight subjects with mild, uncomplicated hypertension. A single oral dose of clonidine (0.3 mg) was given before and after 1 week of therapy with hydrochlorothiazide, 50 mg, and amiloride, 5 mg, taken daily. Changes in mean arterial pressure, heart rate, plasma norepinephrine and epinephrine levels, and plasma renin activity were assessed. Diuretic treatment caused a significant weight loss, increased plasma renin activity, and reduced serum potassium concentration but did not significantly alter the absolute reduction in mean arterial pressure caused by clonidine. Absolute clonidine-induced reduction in plasma renin activity after diuretic treatment was three times greater than before treatment, although percent changes were similar. Before diuretic therapy, clonidine significantly reduced the level of norepinephrine (absolute and percent change). After diuretic treatment, clonidine failed to suppress norepinephrine, and the difference from prediuretic changes was significant. The level of epinephrine was not altered significantly either by diuretic treatment or clonidine. These results indicate that diuretic therapy alters the clonidine-activated mechanism for reduction of arterial pressure through a shift from overall suppression of sympathetic tone to pathways that are more restricted to renal tone. This shift may be due to changes in fluid or electrolyte balance that alter the action of alpha 2-adrenergic receptor-mediated pathways. Use of the clonidine suppression test for the diagnosis of pheochromocytoma may give false-positive results in diuretic-treated patients.
Hypertension 1986 Apr
PMID:Diuretic treatment alters clonidine suppression of plasma norepinephrine. 351 47

After a brief introduction on the problems involved in the interpretation of long-term trials, the methods and the results of large clinical trials, on cardioprotection (defined as the ability of a drug to reduce mortality from all causes or fatal cardiovascular events) are reviewed, with the aim of providing useful clinical information for the treatment of the hypertensive patients. At the end of the review the author draws the following conclusions: The benefits of antihypertensive therapy reported in male patients suffering from severe hypertension are such that further controlled trials with placebo are not acceptable from an ethical point of view. The incidence of fatal and non fatal cardiovascular events is relatively low in mild uncomplicated hypertension but increases three-fold in the presence or organ involvement. A statistically significant reduction of mortality from all causes and of fatal cardiovascular events has been obtained in such patients by means of antihypertensive treatment in the Australian trial, contrary to the results of the MRC trial and the Oslo study. Furthermore, the HDFP trial has shown that mortality from all causes an fatal cardiovascular events are less frequent among patients in stepped care than among those in referred care. The EWPHE trial has demonstrated that antihypertensive treatment reduces non fatal complications and probably reduces mortality in elderly hypertensive patients. Diuretics, sympatholytics and beta-blockers have been used in the large trials on cardioprotection. When several trials prove the equivalence of drugs of different efficacy and safety, it is acceptable to extend the results obtained with such drugs to the therapeutic class they belong to. An example is represented by the results of the MRC and IPPPSH trials on cardioprotection with beta-blockers in male non-smokers suffering from mild-moderate hypertension.
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PMID:[Cardiac protection and antihypertensive therapy: facts and theories]. 352 4

We randomized patients with severe hypertension in the Medical Intensive Care Unit to a treatment regimen of oral nifedipine or intravenous nitroprusside. Patients treated with nifedipine achieved a sustained reduction in diastolic blood pressure to less than or equal to 120 mm Hg in an average of less than five hours. Patients treated with nitroprusside achieved a similar reduction in 14 hours (p less than 0.05). Treatment with nifedipine was less expensive and required less time in the ICU than treatment with nitroprusside and was accompanied by no associated increase in morbidity or mortality. Oral nifedipine can be used as an alternative to intravenous nitroprusside in severe uncomplicated hypertension.
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PMID:A randomized comparison of nifedipine and sodium nitroprusside in severe hypertension. 353 Jun 45

The cardiovascular response to dynamic exercise is generally normal in patients with mild hypertension, but the response to isometric exercise may be increased, with a greater degree of vasoconstriction. The exercise-induced rise of pressure is affected little by most antihypertensive medications; with beta blockers, the response to dynamic exercise may be diminished, but to isometric exercise it may be enhanced. There is increasing evidence that regular dynamic exercise may attenuate the development of hypertension and lower blood pressure in patients with mild hypertension. For patients with mild, uncomplicated hypertension, the benefits of exercise appear to out-weigh the risks.
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PMID:Exercise and hypertension. 355 1

Thiazide diuretics are considered to be the cornerstone of contemporary antihypertensive therapy and are generally recommended as the initial treatment for patients with mild to moderate, uncomplicated hypertension. Hypokalemia and hypomagnesemia are two metabolic alterations that are associated with long-term thiazide therapy. Thirty-five patients (20 with low renin status and 15 with normal renin status) with mild to moderate essential hypertension were treated with hydrochlorothiazide in a dose-titration experiment after a four-week lead-in period. The initial daily dose was 12.5 mg; this was increased at four-week intervals to 25 mg, 37.5 mg, and 50 mg daily. The endpoint dose of this titration was that dose at which the patient's blood pressure normalized, or the dose of 50 mg, if that dose was reached. Patients were maintained on their endpoint dose of hydrochlorothiazide for 24 weeks of continuous thiazide monotherapy beyond the dose titration. The serum potassium and serum magnesium levels during the control period were 4.4 +/- 0.2 mmol/liter and 2.30 +/- 0.08 mg/dl, respectively. During dose titration, each incremental increase of hydrochlorothiazide produced a decrease in blood pressure and a stepwise decrease in serum potassium and magnesium levels. A previously reported study involving 38 patients with mild to moderate hypertension (22 with low renin status and 16 with normal renin status) used similar methods to study higher-dose thiazide therapy. An initial dose of 50 mg daily of hydrochlorothiazide was administered; this was increased at four-week intervals to 100 mg, 150 mg, and 200 mg. The serum potassium and serum magnesium levels during the control period were 4.5 +/- 0.2 mmol/liter and 2.1 +/- 0.18 mg/dl, respectively. In the hypertensive patients with normal renin status, doses of hydrochlorothiazide greater than 50 mg did not result in further blood pressure lowering effects; however, the undesirable effects of hypokalemia and hypomagnesemia continued to be manifested and increased at higher doses of hydrochlorothiazide. Thirty-eight patients who had previously experienced hypokalemia, palpitations, or cardiac arrhythmia were placed on hydroclorothiazide therapy for one to three months and were monitored for arrhythmias after treadmill exercise. The occurrence of premature ventricular contractions correlated significantly with the decrease in serum potassium (r = 0.73, p less than 0.001) and serum magnesium (r = 0.68, p less than 0.001) levels during hydrochlorothiazide therapy and with the product of the change of the two cations (r = 0.81, p less than 0.001).
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PMID:Thiazide treatment of hypertension. Effects of thiazide diuretics on serum potassium, magnesium, and ventricular ectopy. 370 51

Although hypertensive patients have been shown to have a higher prevalence of arrhythmias during ambulatory monitoring when treated with diuretic drugs than when untreated, the effects of maximal aerobic stress on arrhythmia frequency in such patients is unknown. The incidence of arrhythmias during graded maximal treadmill exercise in a group of 68 subjects with mild, clinically uncomplicated systemic hypertension treated chronically with diuretics alone for a median of 4.5 years was compared with that in an age-matched normotensive control group. The prevalence of exercise-induced arrhythmias was higher in the group treated with diuretics than in the control group, 57% vs 38% (p less than 0.05). This difference was entirely due to the higher incidence of isolated atrial or ventricular premature complexes in the diuretic-treated patients, 44% vs 26% (p less than 0.05). There was no difference in the incidence of frequent (more than 10% of beats) or complex supraventricular or ventricular premature complexes between the diuretic-treated and control groups. Within the diuretic group, no difference in the incidence of simple or complex arrhythmia was found between men and women, between those with and those without rest or exercise-induced electrocardiographic abnormalities or between those with a serum potassium level of less than 3.7 mEq/liter vs those with a level of 3.7 mEq/liter or greater. Thus, patients with uncomplicated hypertension treated with chronic diuretic monotherapy do not appear to be at increased risk for major arrhythmias during aerobic exercise.
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PMID:Exercise-induced arrhythmias in diuretic-treated patients with uncomplicated systemic hypertension. 382 52

To evaluate the efficacy of acebutolol, 400-600 mg/day in elderly hypertensive patients, and to compare it with hydrochlorothiazide 25-50 mg/day, 45 patients with mild-moderate uncomplicated hypertension were treated for 6 weeks in a multicentre, single-blind, randomized, crossover trial. Acebutolol decreased supine systolic blood pressure from 186.5 to 162.7 mmHg and diastolic blood pressure from 107.4 to 92.4 mmHg. Hydrochlorothiazide decreased systolic blood pressure from 185.0 to 166.4 and diastolic blood pressure from 107.2 to 96.4. There was no difference between the effects of acebutolol and hydrochlorothiazide on blood pressure during the trial. Both drugs proved to be safe and effective antihypertensive agents, provided the major contraindications for their use were taken into account. Beta-blockade by acebutolol was highly effective in treating mild-moderate arterial hypertension in the elderly.
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PMID:Multicentre comparison of the antihypertensive effect of acebutolol and hydrochlorothiazide in uncomplicated mild-moderate hypertension in the elderly. 390 26

The beta-adrenergic receptor blocking drugs have been in use for the treatment of hypertension for almost two decades. Although the mechanism of their antihypertensive action still is not precisely known, they have become an established major class of therapy for the disease. Most agents produce an immediate reduction in heart rate and cardiac output, later followed by a reduction in pressure. The exceptions include: those agents that possess intrinsic sympathomimetic activity and produce little reduction in heart rate and output; and labetalol, an agent that reduces pressure immediately (associated with the cardiac effects) because it possesses alpha- as well as beta-adrenoceptor blocking effects. Just because a beta-blocking drug reduces cardiac output significantly, it does not follow that renal blood flow will decrease; this depends upon the number and affinity of receptors in the renal circulation. Most beta blockers (including labetalol) reduce renal vascular resistance in patients with uncomplicated hypertension. Other actions of this class of adrenoceptor blocking agents are discussed. As we learn more of the physiologic effects of adrenoceptor blocking agents, there is no doubt that we shall gain more insight into the underlying mechanisms of hypertensive diseases as well as their pharmacologic properties.
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PMID:Pharmacologic and physiologic considerations of adrenoceptor blockade. 613 19

The acute and long-term haemodynamic effects of pindolol, practolol, alprenolol, oxprenolol, acebutolol, penbutolol, metoprolol, atenolol, propranolol and timolol in patients with uncomplicated hypertension as reported in the literature were analysed. The long-term effects of these beta-adrenoceptor antagonists on plasma renin activity and the concentration of noradrenaline in plasma were also reviewed. In spite of the many pharmacological and physicochemical differences the drugs appeared to have a hypotensive effect of approximately equal magnitude. The degree of cardiodepression and the suppression of plasma renin activity as exerted by the different beta-blockers were inversely correlated with their pharmacologically defined degree of intrinsic sympathomimetic activity (ISA). The increments in vascular resistance acutely after administration of a beta-blocker are proportional to the degree of cardiodepression, suggesting that increased vasoconstrictor nerve activity mediated through the baroreflex had prevented an acute fall in arterial pressure in response to a given fall in cardiac output. After long-term therapy the inverse correlation between changes in cardiac output and changes in vascular resistance is shifted to a lower level of vascular resistance. Plasma renin activity and vascular resistance are inversely correlated during long-term beta-blocker therapy for hypertension. Consequently, the fall in vascular resistance underlying the hypotensive effect of beta-blockers cannot be explained by suppression of plasma renin activity. Thus, cardiodepression and renin suppression are not essential for the hypotensive effect of beta-adrenoceptor antagonists. The accessibility of the central nervous system to the different beta-blockers neither determines the time of onset of blood pressure reduction nor the magnitude of this effect. If it is neither the blockade of postsynaptic beta-adrenoceptors in the heart or on juxtaglomerular cells, nor the blockade of central beta-receptors that can be held responsible for the blood pressure lowering efficacy of beta-adrenoceptor antagonists, one is left with the remaining possibility that blockade of presynaptic beta-receptors underlies the vasodilator and antihypertensive action of these drugs. Changes in the concentrations of noradrenaline in plasma are compatible with this supposition, provided that changes in clearance of noradrenaline from plasma are taken into account.
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PMID:Haemodynamic consequences of intrinsic sympathomimetic activity in relation to changes in plasma renin activity and noradrenaline during beta-blocker therapy for hypertension. 613


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