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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

The treatment response to beta-adrenoceptor blocking drugs was compared in two groups of patients with primary (essential) hypertension and different renin levels. Each group consisted of 25 patients and was equally distributed regarding age, severity and stage of hypertension. In the first group (group 1), the mean upright plasma renin activity was 0.8 ng ml-1h-1 (range 0.3 to 1.5) and the patients were considered to have low renin hypertension. In the other group (group 2) the patients had a mean plasma renin activity of 2.1 ng ml-1h-1 (range 1.1 to 5.1) and were considered to have normal to high renin hypertension. In both groups the patients were initially treated with beta-blocking drugs; in group 1 with a beta-blocker corresponding to an average dose of 311 mg propranolol a day for at least eight weeks and in group 2 with propranolol 320 mg a day in a fixed dose for eight weeks. The hypotensive response differed significantly between the two groups (p less than 0.001). In group 1 the pretreatment blood pressure was 197/117 mm Hg supine and 198/120 mm Hg standing. During treatment blood pressure decreased only 5/3 mm Hg supine and 9/5 mm Hg standing. The pretreatment blood pressure in group 2 was 187/114 mm Hg supine and 186/117 mm Hg standing. Beta-blocking therapy reduced blood pressure 36/23 and 34/18 mm Hg, respectively (both p less than 0.001). Pulse rates fell significantly in the two groups, both in the lying and standing positions. In 17 patients with low renin hypertension (group 1), a volume-depleting drug was added (spironolactone, 14 patients; thiazides, 3 patients) and this achieved a marked fall in blood pressure levels of 38/16 mm Hg supine and 37/19 mm Hg standing (both p less than 0.001). These results suggest the following: (1) Most patients with normal to high plasma renin activity respond well to moderate doses of propranolol. (2) Propranolol given in the same doses is almost without antihypertensive effect in patients with low renin hypertension. (3) A volume factor may be operating in patients with low renin hypertension since a hypotensive effect is demonstrated after the addition of volume-depleting drugs. (4) Determination of plasma renin activity with adequate methods can predict the treatment response to hypotensive agents.
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PMID:Different antihypertensive effect of beta-blocking drugs in low and normal-high renin hypertension. 1 4

1 Cardioselective and non-selective beta-blockers affect to a different degree several aspects of the circulatory homeostasis. The evidence available in this regard has been evaluated and the possible clinical importance of these differences has been discussed. 2 Venous return in partly regulated by beta-receptors (possibly of the beta 2 type) in the venous resistance vessels. Differences in blockade of venous return by the two classes of beta-blockers may, therefore, influence the degree of increase in left ventricular size, left ventricular end diastolic BPs and stroke volume during beta-blockade. 3 At the first part of the dose-reponse curve, non-selective beta-blockers seem to block more effectively renin release than cardioselective beta-blockers. 4 The direction and the extent to which beta-blockers 'directly' affect total peripheral resistance (TPR), is determined by the resultant of the degree of decrease in TPR by blockade of renin release and the extent of the increase in TPR by blockade of the beta 2-receptors in the arteriolar wall. 5 The clinical relevance of these differences could be that--especially in the low doses range--non-selective beta-blockers may be more 'safe' in patients with compromised cardiac function and may be more appropriate for the therapy of high renin hypertension than cardioselective blockers, whereas the latter may be more appropriate for the majority of hypertensive patients who have low to normal renin hypertension.
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PMID:Possible significance of the pharmacological differentiation of beta-blockers for therapy of hypertension. 3 72

In patients with essential hypertension a gradual decrease in basal and stimulated renin secretion was found with increasing age. Stimulated plasma aldosterone decreased similarly; however, the observed changes were less pronounced. Young patients (less than 35 years) with high renin hypertension had lower diastolic blood pressure than patients with low renin hypertension in the same age group. Contrary to these findings, a markedly higher diastolic blood pressure was observed in patients over 35 years of age with high renin hypertension than in the group of patients with low renin hypertension. These results indicate that neither high nor low renin essential hypertension patients represent homogeneous groups. Furthermore, the dissociation between changes in renin activity and plasma aldosterone points to a disturbed relationship between the renin angiotensin system and aldosterone secretion in essential hypertension.
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PMID:[Plasma renin activity and plasma aldosterone in essential hypertension: effect of age and diastolic blood pressure]. 101 95

The anti-hypertensive effect of spironolactone and thiabutazide was tested on 47 unselected patients with primary hypertension. They were divided into two groups according to the change in plasma-renin activity in response to furosemide administration: those with and those without response to stimulation, and sub-groups with low, normal or high plasma-renin activity (low renin hypertension; normal renin hypertension; high renin hypertension). During both 4-week treatment periods there was a distinct fall in systolic blood pressure, most marked in the patients without plasma renin stimulation (after spironolactone of about 26.2 mm Hg, after thiabutazide 29 mm Hg), the diastolic pressure fall being only slight in all groups (about 5-10 mm Hg). The plasma-renin activity and plasma-aldosterone concentration increased in all groups, after both spironolactone and thiabutazide three-to fourfold compared with the basal value, even in patients without change in plasma-renin activity after furosemide injections. Serum sodium content decreased after administration of spironolactone, increasing again after subsequent thiabutazide administration. Serum potassium content increased after spironolactone, decreasing after thiabutazide. There was no significant difference between either individual groups or different treatment periods with spironolactone or thiabutazide as far as weight, urine volume or electrolyte excretion in 24-hour urine was concerned.
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PMID:[Spironolactone and thiabutazide in the treatment of essential hypertension (author's transl)]. 116 22

Page kidney is caused by the accumulation of blood in the perinephric or subcapsular space, resulting in compression of the involved kidney, renal ischemia, and high renin hypertension. Most patients are young hypertensives with a remote history of blunt trauma to the abdomen or back. We describe a case of acute Page kidney following a renal biopsy in a patient with underlying IgA nephropathy. In addition to the new-onset hypertension, this patient developed a significant decline in renal function due to the inability of the contralateral diseased kidney to compensate. Magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound were valuable in making this diagnosis. Medical and surgical therapeutic options were considered. This report also reviews all previously described cases of Page kidney.
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PMID:Page kidney: case report and review of the literature. 195 41

This paper describes clinical features of high renin hypertension in the elderly. Peripheral plasma renin activity ranged from 0 to 20.1 ng/ml/hr in 59 hypertensive in-patients aged 70 to 86. The patients were divided into 2 groups: 9 cases with plasma renin activity greater than or equal to 3.0 ng/ml/hr (high renin group) and the remaining 50 with plasma renin activity less than 3.0 ng/ml/hr (control group). The development of hypertension differed between the 2 groups. Six of the high renin group (66.7%) had a history of acceleration of previously mild hypertension, while only 3 of the control group (6.0%) had this history (p less than 0.01). The frequencies of high diastolic blood pressure (greater than or equal to 120 mmHg), massive proteinuria (at least 3.0 g/day), hypokalemia (serum potassium less than or equal to 3.0 mEq/L) and high serum cholesterol (greater than or equal to 250 mg/100 ml) were significantly greater in the high renin group than in the control group (p less than 0.01, respectively). Renovascular hypertension was suspected in 6 patients from the high renin group (66.7%), as compared with 1 of the control group (2.0%) (p less than 0.001). There was massive proteinuria in 3 of 6 patients with renovascular hypertension in the high renin group and 2 showed nephrotic syndrome. Thus, two-thirds of the elderly patients with high renin hypertension had probable renovascular hypertension with a history of rapid progression of hypertension.
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PMID:High renin hypertension in the elderly. 329 10

The abrupt cessation of antihypertensive medication is usually without immediate consequence but may be associated with symptoms and signs of enhanced sympathetic activity, severe hypertension, morbid ischemic cardiovascular events, or death. This syndrome is more common after discontinuation of high doses of centrally acting antiadrenergic and beta-adrenergic blocking drugs or combination antihypertensive therapy, but it also occurs with numerous antihypertensive agents. Predisposing factors include ischemic heart disease, severe hypertension, renovascular or high renin hypertension, and high doses of multiple antihypertensive drugs. Gradual tapering of antihypertensive medications over seven to ten days will prevent symptoms and marked elevation of blood pressure. Should a discontinuation syndrome develop, re-administration of the drug previously discontinued is the most appropriate treatment.
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PMID:Abrupt discontinuation of antihypertensive therapy. 611 86

Whilst plasma renin values are elevated in a minority of patients with essential hypertension, there is no indication that high renin hypertension is a distinct entity and even where renin levels are elevated, they are usually less than those observed in renovascular hypertension. It is still possible for the renin-angiotensin system to be important, if blood pressure is maintained by renin activity within the arterial or arteriolar walls. Accordingly, renin-like activity or rat aortic wall homogenate and plasma renin concentrations were measured simultaneously. Both plasma and aortic renin (measured with an incubation pH of 6.5) rose in salt-depleted and fell in salt-loaded rats. Both were elevated in Goldblatt 2-kidney hypertension. However, aortic renin fell gradually over 24 h after bilateral nephrectomy, whilst plasma renin had reached its nadir by 1 h. To assess the importance of arterial as opposed to plasma renin the renin-angiotensin system was blocked with the converting enzyme inhibitor Sq20881. A blood pressure fall attributable to renin-angiotensin blockade could be demonstrated for at least 6 h after bilateral nephrectomy. This supports the hypothesis that renin in the arterial and arteriolar wall, rather than plasma renin, is responsible for blood pressure maintenance. Nevertheless, in steady state conditions such as essential hypertension, plasma and arterial renin are closely related.
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PMID:Vascular renin in hypertension. 615 22

Microangiography of end-stage kidneys in relation to high renin hypertension. 15 patients with end-stage renal disease (ESRD) and maintained on chronic hemodialysis were studied with respect to hypertension, the plasma renin activity (PRA) and microangiography of endstage kidneys which were removed for various reasons. The microangiographic patterns were classified into three according to characteristic findings: The first one was characterized by gross dilatation of interlobular arteries and afferent arterioles with poor opacification of efferent and peritubular vessels. This pattern was designated as type 1 (Fig. 1, 2.) Another pattern had total irregularity of renal vascular architectures and differentiation of cortical arteries were impossible. This was classified as type 2 (Fig. 3, 4.) The third one which was grouped as type 3 was characterized by good and fine vascularity of cortical vessels without evidence of obstruction (Fig. 5, 6.) These findings were confirmed by histological studies. All 5 patients with uncontrollable hypertension had type 3 kidneys. Their PRA were abnormally high, but normalized after bilateral nephrectomy. It was suggested that intractable hypertension in patients with ESRD may be an evidence of relatively well preserved cortical circulation despite of extensive parenchymal destruction as seen in type 3 kidneys, in which intensive hemodialysis and ultrafiltration will result in volume depletion, decrease in renal perfusion pressure and excessive renin secretion from the remaining nephrons.
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PMID:Microangiography of end-stage kidneys in relation to high renin hypertension. 636 79


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