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

Present knowledge of the mechanisms regulating release of renin is reviewed with particular emphasis on neural factors. Evidence is given for a direct effect of renal innervation on beta adrenergic receptors in juxtaglomerular cells, and for the involvement of reflex release of renin in conditions such as tilting and acute salt depletion. Participation of neural and nonneural mechanisms of control is also shown to occur in other conditions, such as aortic constriction and hemorrhage. The view is held that neural sympathetic factors might explain some of the renin disturbances found in essential hypertension. First, in patients with high renin hypertension part of the hypertension is renin-dependent, and these pressor levels of renin seem to be neurally induced since they can commonly be suppressed by beta adrenoreceptor blocking agents. Second, the hypothesis is presented that patients with low renin hypertension, at least those who have no volume disturbance, have a blunted sympathetic control of renin release. Therefore a sufficiently precise test of sympathetic activity, and possibly of body fluid volumes, should be associated with renin profiles for a better understanding of the pathophysiology of arterial hypertension and as a better guide to therapeutic management. Indeed, most of the available antihypertensive drugs act on sympathetic activity, body fluid volume or renin, and this multifaceted profile would provide more rational guidelines for treatment.
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PMID:Control of renin release: a review of experimental evidence and clinical implications. 0 64

Primary aldosteronism and renovascular hypertension are two different diseases in which renin determinations are necessary for establishment of diagnosis or therapeutic procedure. Low renin values which are not stimulated by acute stimuli combined with elevated plasma aldosterone concentrations confirm the diagnosis of primary aldosteronism. When in a patient with proven renal artery stenosis a significant difference in renal venous renin activity is observed between the two kidneys, a connection between hypertension and renal artery stenosis is likely when in addition the renin secretion of the unaffected kidney is suppressed. A favourable outcome for surgery can be predicted when the individual clinical picture in such a case is also considered. A similar view also holds for the connection between hypertension and unilateral small kidney not due to renal artery stenosis. In essential hypertension the plasma renin level makes it possible to a certain extent to predict whether a patient will benefit from diuretics or from beta-blocking agents. Despite this experience, however, renin determinations are not indicated in every case of essential hypertension. It has not been proven that the prognosis of this disease is improved by renin oriented monotherapy rather than by effective treatment with other antihypertensive agents.
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PMID:[The value of renin determination in the diagnosis of hypertension]. 0 81

When pathophysiological and pathogenetic aspects of hypertension are taken into consideration with special regard to diabetes mellitus the exhaustion of the "insulin enhancement" within the cerebrovisceral functional systems (Baumann) are discussed and the authors enter possible connections of diabetes mellitus to the renin-angiotensin-aldosterone system. After explanation of the diabetogenic and antidiabetogenic pharmacodynamic qualities of the antihypertensive drugs adequate therapeutic recommendations are proposed summarized in a figure. The authors conclude that for the present antihypertensive therapy in diabetics taking into consideration the references reported on there are sufficient possibilities of treatment for all degrees of severity of hypertension. Such preparations as Rausedan, Disotat, Dopegyt appear as particularly suitable; moreover, the beta receptor blockers, Haemiton, Depressan as well as Guanitil and Pargylin prove to be possible or without disadvantage, respectively. Especially when diuretics are described an exact control of the metabolism should be carried out.
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PMID:[Treatment of hypertonus in diabetes mellitus]. 0 29

The effect of timolol versus propranolol on hypertension, hemodynamics, and plasms renin activity was evaluated in 20 men. After two weeks of placebo, 11 men received timolol 30 to 60 mg daily, and nine men received propranolol, 240 to 480 mg daily, for five weeks in a double-blind randomized study. The 20 men then received placebo again for two weeks. Right heart catheterization was performed in all 20 patients after two weeks of the first placebo and after five weeks of timolol or propranolol. Equipotent doses of timolol and propranolol were equally effective in significantly lowering supine and upright systolic and diastolic blood pressure and heart rate recorded on an outpatient basis. Equipotent doses of timolol and propranolol caused similar hemodynamic effects including similar significant depression of cardiac index. Equipotent doses of timolol and propranolol caused similar marked depression of plasma renin activity. The hypotensive action of timolol and of propranolol was unrelated to their effect on plasma renin activity.
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PMID:Effect of timolol versus propranolol on hypertension and hemodynamics. 0 61

Plasma renin activity (PRA) was measured in 38 cases of aortitis syndrome. The values of resting peripheral vein blood PRA were 32.2 +/- 4.2 (SE) mmug/ml. These values were 3 times higher than those of normal subjects. Hypertension due to renal arterial stenosis was observed in 18 cases. Their resting PRA values were 41.2 +/- 6.0 mmug/ml, while in the remaining 20 patients without renovascular hypertension those values were 24.2 +/- 5.4 mmug/ml. The patients belonging to aortic arch type or extensive type had 2 times higher PRA values than those of abdominal type. The patients with stenosis or obstruction of common carotid arteries had significantly higher PRA values than the patients without these lesions. Hyperresponse of renin secretion to upright posture was also observed in the same patients with carotid artery stenosis. Abnormal renin release in Takayasu's arteritis disappeared after denervation of the carotid sinus nerve. The present study suggests that the unstable state of carotid sinus reflex is the main cause for the hypersecretion of renin.
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PMID:Elevated plasma renin activity in aortitis syndrome. 0 6

Basing on the literature data and their own observations of patients with chronic hemodialysis the authors have analysed the pathogenesis, course, hemodynamic shifts and possibilities of purposeful treatment in terminal uremia. Besides two variants of the hypertension course (controlled and noncontrolled), a third type has been revealed--hypertension difficult to control, in the pathogenesis of which, as well as in the noncontrolled variant, an important role is played by the activization of the renin-angiotensin system. Hemodynamic mechanizms of an abrupt change in the arterial pressure (acute hypotension and hypertensive crisis) in the process of hemodialysis are analysed.
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PMID:[Arterial hypertension and chronic hemodialysis]. 0

The effects of penbutolol (Hoe 893 d), a new non-selective beta-receptor blocking agent, were studied in 5 patients with moderate hypertension. Initially, it was shown that 2-4 mg given orally once or twice daily tended to lower blood pressure and pulse rate, both at rest and following submaximal work. In prolonged trials (3-8 months) 4-60 mg/day were required to produce an acceptable antihypertensive effect. Penbutolol had no effect on the normal increase in plasma noradrenaline and adrenaline on standing, nor did it alter basal urinary catecholamine excretion. Submaximal work caused no significant change in plasma catecholamines before treatment, but there was a marked rise both in plasma noradrenaline and adrenaline during treatment with penbutolol. In short term studies there was a fall in plasma renin by 4 hours after oral administration of penbutolol 2-4 mg, which persisted for 24 hours. Prolonged treatment with penbutolol 20-30 mg twice daily inhibited renin production under basal conditions and following submaximal work, as well as lowered basal urinary aldosterone excretion. In one patient slight asthmatic symptoms appeared after treatment for 3 months with penbutolol. In other respects penbutolol was well tolerated.
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PMID:Long term treatment of moderate hypertension with penbutolol (Hoe 893d). I. Effects on blood pressure, pulse rate, catecholamines in blood and urine, plasma renin activity and urinary aldosterone under basal conditions and following exercise. 0 98

The effect of insulin-induced hypoglycemia on the blood levels of catecholamines and renin activity has been studied in five patients with moderate hypertension before and after treatment for 3 - 8 months with penbutolol (PEN) 20 - 30 mg twice daily. Penbutolol caused no change in fasting blood glucose level. Insulin o.1 IU per kg body weight i.v. reduced blood glucose concentration by approximately 50 per cent after 30 - 45 min, both before and during treatment with penbutolol. Hypoglycemia prior to medication was accompanied by a marked increase in the production of adrenaline and a minor increase of noradrenaline in all five patients. During treatment the response of adrenaline to hypoglycemia was reduced in four patients and the data was inconclusive in one. Basal renin activity was rather low in three patients, within the normal range in one and relatively high in one. Before penbutolol the hypoglycemia-induced increase in catecholamine production caused no change in plasma renin activity in the three patients with low basal levels, whereas a marked increase was observed in the other two. During medication plasma renin activity remained unchanged on induction of hypoglycemia regardless of the catecholamine response. Despite the marked increase in plasma adrenaline following insulin-induced hypoglycemia, no statistically significant increase in pulse rate was recorded.
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PMID:Long term treatment of moderate hypertension with penbutolol (Hoe 893d). II. Effect on the response of plasma catecholamines and plasma renin activity to insulin-induced hypoglycemia. 0 1

Blood pressure (BP), plasma renin concentration (PRC), plasma renin substrate concentration (PRSC) and exchangeable sodium (ES) have been studied in 27 patients undergoing regular hemodialysis because of end-stage renal disease. PRC was significantly higher in the hypertensive than in the normotensive patients. The pattern of PRSC was similar in the groups of patients but with a marked individual variation. ES was slightly lower in the hypertensives than in the normotensives but the difference was not statistically significant. Multiple regression analysis demonstrated a significant correlation between mean BP, the natural logarithm of PRC and ES, but the effect of ES was negligible. PRC was negatively correlated to ES in all patients, including the hypertensives. These results strongly suggest that the renin-angiotensin system is the most important factor involved in the pathogenesis of hypertension in end-stage renal disease, when sodium balance is adequately controlled. A clinical application of the predictive value of PRC concerning the effect of bilateral nephrectomy on hypertension is outlined.
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PMID:Hypertension in end-stage renal disease. The relationship between blood pressure, plasma renin, plasma renin substrate and exchangeable sodium in chronic hemodialysis patients. 1 Jul 15

Plasma renin levels have been used to discriminate between different forms of hypertension, but how to define the normal range of plasma renin levels has not been agreed upon. Sodium depletion stimulates renin release. Evaluation of plasma renin would, therefore seem possible only in relation to sodium balance. Plasma renin concentration and concurrent daily sodium excretion were determined in 33 healthy normotensive subjects (control group) ingesting high, normal and low sodium diets. A well-defined hyperbolic relationship was found between the two variables indicating that the physiologic level of plasma renin concentration depends on the state of sodium balance. An increase in plasma potassium concentration may reduce plasma renin concentration, but this appeared to be overruled by the stimulating effect of sodium depletion. To examine whether beta-adrenergic stimulation contributes to the increase in plasma renin concentration during sodium depletion, the relationship between plasma renin concentration and concurrent sodium excretion was studied during beta-receptor blockade with propranolol. In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity.
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PMID:Effect of sodium depletion on plasma renin concentration before and during adrenergic beta-receptor blockade with propranolol in normotensive man. 1 Jul 25


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