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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Indomethacin was administered alone or in addition to either diuretic or propranolol therapy to three groups of patients with essential hypertension on a free sodium diet. 2. Indomethacin administration reduced renin secretion by about 30% in untreated uncomplicated hypertensive patients and by about 75% in those whose renin secretion had either been stimulated or suppressed by maintained diuretic or beta-adrenoreceptor-blockade therapy. 3. Indomethacin administration produced no net effect on blood pressure in untreated patients with uncomplicated hypertension but it blunted or reversed the antihypertensive effect of either diuretic or propranolol therapy. 4. Salt and water retention may be an important factor in the blood pressure-raising effect of indomethacin during diuretic or propranolol therapy: In addition, prostaglandin synthesis may be important in counteracting increased alpha-adrenergic tone, which may limit the blood pressure-lowering effect of beta-adrenoreceptor-blockade. 5. Because of these interactions and their pressor potential indomethacin should be used with caution when combined with either diuretics or beta-adrenoreceptor blockers.
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PMID:Effects of indomethacin alone and during diuretic or beta-adrenoreceptor-blockade therapy on blood pressure and the renin system in essential hypertension. 28 51

The pivotal role of the kidney in sustaining hypertension from any source or etiology is becoming increasingly clear. The possibility that the renal vasculature participates not only in the pathogenesis of renal vascular hypertension, but also in that of essential hypertension, has been the subject of continuing interest for 40 years. Evidence that a functional abnormality resulting in increased renal vascular tone is present in about two-thirds of patients with uncomplicated essential hypertension is reviewed, along with more circumstantial evidence that sympathetic nervous system activity operating on the renal vasculature is responsible. Two additional groups of patients in whom a characteristic abnormality of the renal vasculature is present have also been identified. In one group there is severe hypertension which is resistant to most forms of antihypertensive therapy but which is especially responsive to propranolol. In these patients renal blood flow and glomerular filtration rate are reduced, renin secretion rate is increased and the renal vessels are resistant to vasodilators, suggesting the presence of advanced organic arteriolonephrosclerosis, as a complication of long-standing, severe hypertension. The renal lesion, in turn, contributes to the increasing severity of the process. In a second group of patients, generally young and with uncomplicated hypertension, renal blood flow is inappropriately increased. In these patients a number of observations on their renal vasculature, renin and aldosterone responses to a volume challenge suggest an abnormality in the perception of extracellular fluid volume. A perfectly normal renal arterial tree, free of organic abnormality or an increase in tone due to active vasoconstriction, is distinctly unusual in essential hypertension.
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PMID:The renal circulation in hypertensive disease. 79 87

Authors assessed correlation between venous blood catecholamines and prostaglandins concentrations before and after inhibition of sympathetic activity by clonidine in patients with primary hypertension or pheochromocytoma. 30 patients with essential uncomplicated hypertension and 11 with pheochromocytoma underwent the study. The control group consisted of 6 healthy volunteers. Serum norepinephrine (NA), epinephrine (A), prostaglandins: PGE2 PGF2 alpha and prostacyclin metabolite -6-keto-PGF1 alpha were determined before and 3 hours after oral administration of 0.3 mg clonidine. Negative correlation was stated between basic serum norepinephrine and 6-keto-PGF1 alpha concentrations in patients with pheochromocytoma, which could indicate prostacyclin metabolism disorders during persistent hypercatecholaminemia . There was no correlation between catecholamines and prostaglandins during the inhibition of sympathetic activity in patients with pheochromocytoma as well as essential hypertension. The positive correlation was observed between changes in serum NA and PGF2 alpha levels in patients with borderline hypertension. Thus, one may suppose, that correlation between na excretion and vasoconstrictive PGF2 proved in acute experiments, becomes evident within the early stage of hypertension also during sympathetic activity inhibition.
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PMID:[Correlations between catecholamines and prostaglandins in patients with primary arterial hypertension and pheochromocytoma in basic conditions and after administration of clonidine]. 208 2

1. In this double-blind randomized study, after a 4-weeks placebo period, 18 patients with mild to moderate primary hypertension were assigned to treatment with either dilevalol (n = 9) daily or atenolol (n = 9) over a period of 3 months. 2. Expiratory flows, lung volumes and airway responsiveness (AR) to methacholine were assessed at the end of the placebo period and after an active treatment of 12 weeks. Blood pressure (BP), heart rate (HR) and ECG were monitored during the methacholine challenges. Twice daily peak expiratory flow rates and respiratory symptoms were recorded on a diary card. 3. No significant effects on ECG, HR and BP were observed after methacholine inhalation. In all but one subjects there was no significant change in expiratory flows, lung volumes or AR throughout the study. Mean FEV1, FVC, PEFR, FRC and PC20 methacholine were unchanged after 3 months of treatment, and not statistically different between patients on dilevalol or atenolol. 4. One subject, without previous history of asthma, developed transient airflow obstruction 8 weeks after beginning dilevalol. 5. Dilevalol and atenolol have no significant effects on pulmonary function and AR in most subjects with no baseline airflow limitation. 6. Airflow obstruction may develop in normal subjects on dilevalol. Methacholine challenges are safe in subjects with uncomplicated hypertension.
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PMID:Comparative effects of dilevalol and atenolol on lung function and airway response to methacholine in hypertensive subjects. 219 11

Careful consideration of all relevant scientific evidence and a critical assessment of data quality show that thiazide diuretics are not cardiotoxic. Of 12 reported trials only two recorded more coronary heart disease events in thiazide-treated patients than in controls. One of these two was a subgroup of a larger study (Heart Attack Prevention in Primary Hypertension, HAPPHY) which found no difference between thiazide-treated and beta-blocker-treated patients. The other, the Oslo study, was too small to allow valid conclusions. Results from a subgroup in the Multiple Risk Factor Intervention Trial (MRFIT) that appeared to supply evidence for thiazide-related cardiotoxicity are suspect when examined critically. Further evidence from 24- to 28-h ECG monitoring does not support the hypothesis that thiazide diuretics, either in the presence or absence of hypokalemia, increase the frequency or severity of ventricular arrhythmias. Reports of a thiazide-induced intracellular magnesium deficiency as a cause of ventricular arrhythmias have also not been confirmed; the development of arrhythmias in acute myocardial infarction appears to be due to an increase in catecholamine levels rather than hypokalemia. There appears to be little evidence to support the assumption that long-term use of thiazide diuretics aggravates or accelerates atherosclerosis of the coronary arteries; any fall in serum cholesterol appears to be transient. For the great majority of patients with uncomplicated hypertension, without a previous myocardial infarction, congestive heart failure, diabetes mellitus or gout, thiazide diuretics appear to be both safe and effective antihypertensive agents.
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PMID:The cardiotoxicity of thiazide diuretics: review of the evidence. 221 84

Although the precise cause of essential hypertension is not known, empiric treatment is indicated to reduce cardiovascular risks. Several pharmacologic classes of a antihypertensive drugs are available to reduce blood pressure, but they do so by different hemodynamic mechanisms. The physiologic therapeutic goal in patients with hypertension is to normalize the systemic vascular resistance without inducing major alterations in the cardiac output. In this study we compared the antihypertensive and hemodynamic actions of nicardipine, a calcium antagonist, with propranolol, a beta-blocking drug. Both drugs were effective in the treatment of hypertension. However, while propranolol therapy decreased the resting and exercise left ventricular ejection fraction and cardiac output, cardiac function was well preserved during nicardipine therapy. It is concluded that both nicardipine and propranolol exert similar antihypertensive actions but that they cause dissimilar hemodynamic consequences in patients with uncomplicated hypertension.
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PMID:Nicardipine and propranolol in the treatment of hypertension: similar antihypertensive but dissimilar hemodynamic actions. 230 Dec 45

Ketanserin is a novel agent that has been shown to be a specific 5-HT2-serotonergic antagonist. It has useful antihypertensive properties. Owing to its unique mechanism of action, it has been suggested that ketanserin may have a favorable effect on tissue blood flow during chronic therapy for hypertension. This double-blind study was designed to evaluate the acute (1 week) and chronic (8 weeks) effects of ketanserin on renal hemodynamic parameters and renin-aldosterone axis in patients with uncomplicated hypertension. Compared to placebo, ketanserin caused a significant blood pressure reduction at the end of the 8-week study period. Despite the reduction in systematic arterial pressure, glomerular filtration rate and renal plasma flow were preserved. Ketanserin therapy induced a slight reduction in plasma renin activity and a marginal increase in the sodium excretion. Although the results of this study are limited by the small number of patients, it appears that ketanserin may have favorable renal hemodynamic effects in uncomplicated essential hypertension.
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PMID:Renal hemodynamic effects of ketanserin therapy in essential hypertension. 244 78

Cytosolic free calcium concentrations determine the magnitude of tension development of smooth muscle cells and are pivotal for regulation of vascular smooth muscle tone and systemic vascular resistance. Elevated free calcium concentrations have been found in platelets from hypertensive patients, and platelet free calcium concentration, possibly an index of vascular smooth muscle cell free calcium concentration, correlated with blood pressure in normotensive and hypertensive subjects. Increased systemic vascular resistance in essential hypertension depends on increased calcium influx. Calcium antagonists lower cytosolic free calcium concentrations mainly through a reduction of transmembraneous calcium influx and are potent arterial vasodilators. High blood pressure is lowered through a reduction of elevated systemic vascular resistance but, in contrast to other direct acting vasodilators, without clinically relevant sympathetic reflex activation. However, subtle changes of sympathetic nervous system activity may codetermine the acute and chronic blood pressure response. Calcium antagonists do not lead to volume retention, because of improved intrarenal hemodynamics and a diuretic effect. Interference with angiotensin and sympathetically mediated vasoconstrictor mechanisms probably also contributes to their antihypertensive effects. This favorable hemodynamic profile renders calcium antagonists suitable for monotherapy of uncomplicated hypertension where they are particularly effective in older patients and also for the therapy of hypertensive crisis.
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PMID:Mechanisms of action of calcium antagonists in hypertension. 245 34

Efficacy and feasibility of antihypertensive monotherapy with the calcium antagonist nitrendipine were investigated in a 6-week open trial in 768 patients with mild to moderate essential hypertension from 191 practicing internists and general practitioners. Previous antihypertensive therapy (n = 501) was withheld for 1 week and therapy then started with nitrendipine 20 mg q.d. If diastolic blood pressure before tablet intake in the morning stayed above 90 mm Hg or fell less than 10 mm Hg, the dose could be doubled to the maximum dose of 20 mg b.i.d. Alternatively, if blood pressure control was good, the dose could be halved to 10 mg q.d. One hundred thirty-four patients discontinued therapy prematurely because of unwanted effects mostly characteristic with dihydropyridines (headaches, flushes, and ankle edema) and mostly within the first 3 weeks. In 72% of the remaining 634 patients, the goal blood pressure was achieved by nitrendipine monotherapy (10 mg q.d. in 8%, 20 mg q.d. in 87%, and 20 mg b.i.d. in 5%) and diastolic blood pressure was between 90 and 95 mm Hg in another 3%. Reductions of blood pressure did not result in changes of heart rate or weight. Nitrendipine was effective in patients of all age groups but patients older than 65 years showed a significantly greater fall of systolic and mean arterial pressure than middle aged or young patients. Nitrendipine's efficacy under conditions of general practice and the high proportion of patients responding to once daily administration appear well suited for first-line therapy of uncomplicated hypertension. The incidence of side effects might have been smaller if therapy had started with a smaller dose.
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PMID:Antihypertensive monotherapy with nitrendipine in general practice. 246 61

Atrial natriuretic peptide (ANP) activity was studied in 33 males with borderline and established essential hypertension. No significant differences of serum ANP concentration were stated in patients with borderline and established uncomplicated hypertension in comparison with the control group.
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PMID:[Atrial natriuretic peptide in patients with primary arterial hypertension]. 253 87


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