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

The saralasin test was performed in 68 hypertensives. A clear-cut dependence of the test results on initial plasma-renin concentration and particular sodium balance was demonstrated. Because of this dependence the saralasin test should be performed only under constant conditions. A mild stimulation of the renin-angiotension system by salt restriction to a mean sodium excretion of 50 mmol daily and 80 mg furosemide by mouth 12 hours before the test seems best. In this way essential and renovascular hypertension could be distinguished with considerable reliability (P less than 0.001). Among patients with essential hypertension one could clearly separate those with high plasma-renin concentration from those with a normal or low one. Among patients with renovascular hypertension those with haemodynamically significant renal artery stenosis could with high probability be distinguished from those with non-effective stenosis. A positive saralasin test without testing the function of the normal contralateral kidney does not provide an indication for operation.
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PMID:[The saralasin test in the diagnosis of hypertension (author's transl)]. 43 89

It has been proposed that measurements of plasma dopamine-beta-hydroxylase (DBH) may allow for assessmetn of adrenergic tone and may elucidate a possible neurogenic contribution to essential hypertension. We performed a series of measurements of DBH in fifty-seven normotensive and fifty hypertensive black and white men in order (1) to compare DBH to selected blood pressure patterns and (2) to evalutate the influence of salt intake, posture and race on plasma DBH. Plasma DBH, measured on unrestricted salt intake with subjects supine, was 42 +/- 4 Units/L in white normotensives, greater (P less than 0.05) than black normotensives (26 +/- 6 Units/L). White hypertensives had greater plasma concentrations of DBH than black (35 +/- 3 VS. 24 +/- 5, P less than 0.05). Normotensives did not differ from hypertensives. Dietary salt restriction and upright ambulation increased plasma DBH activity in hypertensives. Although DBH did not correlate directly with blood pressure, high DBH values were associated with lability of blood pressure in hypertensives but not in normotensives. There are two possible explanations for our results: (1) multiple factors influence plasma DBH activity and plasma levels reflect more than adrenergic function, or (2) essential hypertension is a multifactorial disease and excess sympathetic neuronal activity alone is not sufficient to produce sustained hypertension.
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PMID:Plasma dopamine-beta-hydroxylase activity and blood pressure variability in hypertensive man. 48 18

Around the turn of the century it was observed that low dietary salt consumption is frequently associated with reduction in blood pressure in essential hypertension. It has not been established whether this is a specific effect of NaCl or whether it is an unspecific consequence of the weight loss frequently accompanying low salt intake. Changes of the Renin-Angiotension-Aldosterone system do not seem overly important for the understanding of the original lesion in essential hypertension. Hemodynamic studies demonstrate that increased peripheral (arterial) resistance is characteristic for the disease. It was possible to breed a rat strain with an "anlage" for hypertension which could be unmasked by salt supplements. In humans, essential hypertension is associated with increased salt preference suggesting a genetic factor. This increased desire for salt induces a high salt content of the body including the arterial wall. The hypothesis is being discussed that the stimulating effect of NaCl leads to contraction of the arterial wall inducing increased peripheral resistance - the hallmark of essential hypertension.
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PMID:[Sodium chloride and hypertension (an additional, temporary hypothesis)]. 52 31

22 patients (4 female, 18 male, mean age 47 +/- 10.7 years) with severe essential hypertension (n = 21) and renovascular hypertension (n = 1) were treated with a mean daily dosage of 16.3 +/- 5.1 mg minoxidil for up to 42 weeks. In addition, all patients received a diuretic (hydrochlorothiazide or furosemide) and a beta-blocker (pindolol or propranolol). 8 patients were treated simultaneously with alpha-methyl-dopa. Within one week minoxidil led to a significant reduction in both systolic and diastolic supine blood pressure (p less than or equal to 0.005) from 201.3 +/- 29.0/125.4 +/- 19.2 mm Hg to 172.8 +/- 28.3/106.0 +/- 19.9 mm Hg. The maximum initial blood pressure response was observed after 3 weeks with a mean daily dosage of 12.2 +/- 9.4 mg of minoxidil (160.5 +/- 20.7/99.4 +/- 13.8 MM Hg, p less than or equal to 0.001). Throughout the remaining period a constant and significant reduction in supine systolic and diastolic and upright diastolic blood pressure was achieved (p less than 0.005-less than 0.001) whereas at times systolic blood pressure values could not be lowered significantly. Body weight and pulse rate showed no significant changes throughout the study. In some cases furosemide had to be added by up to 500 mg/day to counteract minoxidil induced water and salt retention. Only moderate doses of beta-blockers were required to prevent a drug induced rise in pulse rate. In these patients a significant change in renal function was not observed. The results show that minoxidil is a potent drug in the treatment of severe essential hypertension.
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PMID:[Minoxidil in treatment resistant hypertension]. 53 65

The kidney has a high capacity to produce a spectrum of different acting prostaglandins (PG). In vivo and in vitro studies have shown that renal formation of PG's, possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. PGE2 formed in the medulla modulates the hydroosmotic action of antidiuretic hormone and influences the kidney's capacity for urine concentration. Renal PG formation is reduced by high NaCl intake and enhanced by low NaCl intake and in hypokalemic states. These findings make renal PG's good candidates for participation in the regulation of salt and water balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal cortical production of vasodilating and renin-stimulating PG's could constitute the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension.
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PMID:Formation and action of prostaglandins in the kidney. 53 77

We have studied the effects of intravenous infusion of saralasin, a competitive antagonist of angiotensin II, in 27 hypertensive patients: 13 had essential hypertension, 14 had renal lesions which involved the renal artery in 9 cases. In essential hypertensives saralasin administration did not significantly lower blood pressure, even after mild salt depletion. It induced a decrease in blood pressure in 7 patients with renal abnormalities (5 with renal artery stenosis, 2 with unilateral parenchymal disease). It may be suggested that in these cases hypertension was dependent, at least partly, on the renin-angiotensin system. In agreement with other investigators, we have found a relationship between the level of plasma renin activity and the blood pressure decrease obtained by saralasin. In patients with unilateral renal artery stenosis, blood pressure decrease was related to renal vein ratio of plasma renin activity.
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PMID:[Clinical usefulness of saralasin in human hypertension (author's transl)]. 64 79

The biochemical processes which transform baroreceptor, beta-adrenergic and macula densa signals into an increase or a decrease of renin secretion are unknown. Evidence is presented that the renal PG system is intimately involved in the mechanisms regulating the release of renin. In vivo stimulation of renal PG synthesis by arachidonic acid (C20:4) or furosemide increases renin release. PG synthesis inhibitors decrease basal renin release and reduce the renin release following stimulation with C20:4, furosemide and renal ischemia. In vitro, C20:4 and the PG-endoperoxides stimulate renin release from the rabbit kidney cortex whereas PGF2alpha inhibits it. This suggests an intrinsic role in the renin release mechanism of PGs, synthesized at or near the juxtaglomerular apparatus. The operation of this PG effect on renin release may depend upon a salt intake related control of PG synthesis and of conversion of PGE2 to PGF2alpha. Increased or decreased renal PG synthesis may also be the primary event leading to elevated or reduced renin levels in some clinical disorders. In Bartter's syndrome, the elevated renin levels may result from an increase in PG synthesis or a decrease of PGF2alpha formation. In benign, uncomplicated essential hypertension, decreased renal PG synthesis or increased PGS2alpha formation may be the primary mechanism which reduces renin release and renal blood flow.
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PMID:Renal prostaglandins in the control of renin. 69 7

We investigated the possibility that variability in classification of patients with essential hypertension into low, normal, or high renin activity subgroups depends on the subject preparation that precedes the measurement of plasma renin activity (PRA). In 47 essential hypertensives, PRA was measured with patients supine and ambulatory who were receiving both an unrestricted dietray sodium intake and a low sodium diet. Additionally, PRA was determined following salt restriction, oral furosemide therapy, and ambulation. These results were compared, using several analytical techniques, to those of a group of age-, race-, and sex-matched normotensive controls. Extreme variability in classification was the rule, with only 28% of patients consistently classified as having normal PRA. No single approach provided maximal detection of both the low and high renin states. We conclude that renin classification of hypertensive patients requires a matched control population and that subtyping appears to be variable depending on diet, posture, and analytical approach.
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PMID:A composite analysis of renin classification methods. 70 73

In order to evaluate the relationship between aldosterone status and the blood pressure-lowering effect of spironolactone, 38 patients with essential hypertension were treated with spironolactone (400 mg/day) during one week in hospital on a rigidly sodium-restricted diet. The degree of hyperaldosteronism was assessed by the aldosterone secretory rate after 5 days of salt loading (315 mmol Na+/day). The mean arterial pressure decreased 5.6% (range, -21 to +8%). When the patients were divided into subgroups with low and normal renin activity, there was no difference in the change in mean arterial pressure (-5.0% and -6.1%). When the patients were divided into three groups with low, normal, and supranormal aldosterone secretory rates, the last group had a significantly greater fall in blood pressure after the spironolactone than the other groups (-1.0, -7.1, -11.1%). Thus there was a correlation between the aldosterone secretory rate after sodium loading and the blood pressure-lowering effect of spironolactone (r = -0.53, p less than 0.01). The blood pressure-lowering effect was not related to changes in body weight, kidney function, or plasma electrolytes. Our findings do not provide solid arguments for the view that the blood pressure-lowering effect of high dose spironolactone is due to its antimineralocorticoid activity, but the correlation between the degree of hyperaldosteronism and the blood pressure-lowering effect strongly suggests that aldosterone does play a role in the genesis or maintenance of the hypertension in these patients.
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PMID:Role of aldosterone in the antihypertensive effect of spironolactone in essential hypertension. 71 23

Hereditary and environmental factors are involved in the pathogenesis of essential hypertension. Obesity, salt intake and stress are predominant among the environmental influences. Autonomous nervous dysfunction, increased contractility of vascular smooth muscle cells and impaired renal handling of sodium are major abnormalities in essential hypertension. At present it cannot be decided if alterations in the activities of systemic or renal hormonal systems reflect primary defects or adaptive changes in the regulation of blood pressure. In any case the kidney is regarded to have a key position in the long term increase of blood pressure in essential hypertension. Recent studies in essential hypertensive patients suggest that renin release decreases as renal vascular resistance increases. Studies from our laboratory have shown that renal prostaglandins are intrinsic to the renin release mechanism from the kidney. Additionally, there is evidence that renal prostaglandin synthesis is disturbed in essential hypertension, either primarily or secondarily, leading to unresponsive renin secretion. Further studies on the interrelationships of other hormonal systems and on hormone-receptor interactions in the vascular wall are necessary to delineate more precisely the mechanisms which are operative in the pathogenesis and manifestation of essential hypertension.
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PMID:[Pathogenetic, pathophysiological and biochemical aspects of essential hypertension (author's transl)]. 72 Oct 54


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