Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 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

Plasma catecholamines, indexes of sympathetic nervous tonicity, were measured simultaneously with renin both supine and after standing plus furosemide in patients with primary hypertension and normotensive volunteers. Seventy percent of hypertensive patients with high renin levels had increased catecholamines compared with a 14% incidence in the combined group with low and normal renin (P less than 0.001). Basal catecholamines were related directly to renin in the hypertensive patients and to blood pressure in the normal (P less than 0.05), but not in the high and low renin subgroups, and inversely to percent increase of catecholamines after standing plus furosemide in hypertensive and normotensive patients (P less than 0.01). Sympathetic nervous hypertonicity may be responsible for the elevation of blood pressure and for the activation of the renin-angiotensin system in patients with high renin hypertension.
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PMID:Increased plasma catecholamines in high renin hypertension. 99 17

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

A 65-year-old man presented proteinuria in the nephrotic range that occurs in the setting of high renin hypertension. Proteinuria persisted after normalizing blood pressure by nifedipine. In contrast, treatment with an ACE-inhibitor (enalapril) resulted in the prompt resolution of the proteinuria. Interestingly, proteinuria relapsed after removing the ACE-inhibition. These observations suggest a causal relation between the overactivity of the renin-angiotensin system in this patient and his proteinuria.
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PMID:Nephrotic-range proteinuria in a patient with high renin hypertension: effect of treatment with an ACE-inhibitor. 148 13

Renin secretion by the kidney is inhibited by an increase in free intracellular calcium concentration. This increase in free intracellular calcium content may be augmented by serum 1,25-dihydroxyvitamin D. In 10 subjects with high renin hypertension, an increase in dietary sodium intake resulted in an increase in urinary calcium excretion (2.5 to 3.4 mmol/L, P = .011) and an increase in serum 1,25-dihydroxyvitamin D (51.2 to 61.0 pmol/L, P = .045). An inverse correlation existed between the change in vitamin D and the change in plasma renin activity (r = -0.765, P = .01). An inverse correlation also existed between the change in plasma renin activity and the change in mean arterial blood pressure (r = -0.757, P = .011). It is postulated that the increase in dietary sodium led to an increase in serum 1,25-dihydroxyvitamin D concentration, which may have contributed to an increase in intracellular calcium concentration, a decrease in renal secretion of renin, and a fall in plasma renin activity. The resultant fall in PRA in part effected the change in blood pressure to the increased sodium intake. Therefore, 1,25-dihydroxyvitamin D may be a mediator in the response of high renin hypertension to increased sodium intake.
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PMID:Interaction of 1,25-dihydroxyvitamin D and plasma renin activity in high renin essential hypertension. 208 Oct 10

We have shown previously that both sinoaortic denervation (SAD) and high renin hypertension in the rat produce a pronounced alteration in the pattern of pressure change during sleep, namely from unchanged to a rise in pressure during synchronized sleep (SS) and from a slight rise to a marked fall during desynchronized sleep (DS). Since acute SAD also produces overactivity of the renin-angiotensin system (RAS), we investigated if this overactivity is essential for the development of the alterations. In rats studied 1 day after SAD (138 +/- 1.0 mm Hg) the MAP rose during SS (+14 +/- 0.7 vs. +1.0 +/- 0.16 mm Hg in the controls) and fell during DS (-27.2 +/- 1.5 vs. 4.9 +/- 0.6 mm Hg in the controls). Captopril-treated rats, studied 1 day after SAD (89 +/- 1.2 mm Hg), also exhibited rise in pressure during SS (+12.3 +/- 0.6 mm Hg) and fall during DS (-12.8 +/- 1.7 mm Hg). Similar alterations were observed in rats studied 10 days after SAD (116 +/- 0.7 mm Hg) when RAS activity was normal (PRA: 1.3 +/- 0.2 vs. 10.4 +/- 2.7 ng AI/ml/h for SAD-1 day); the MAP rose during SS (+6.5 +/- 0.3 mm Hg) and fell during DS (-5.0 +/- 0.9 mm Hg). These data indicate that impairment of the baroreceptor function per se determines the typical alteration in the pattern of pressure change during sleep in the rat.
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PMID:Alteration in baroreceptor function in rats produces typical pressure changes during sleep. 245 78

Subjects with high renin hypertension tend to be sodium-resistant showing paradoxical blood pressure responses to alterations in sodium intake. Of twenty-five subjects with high renin essential hypertension (ten females, 15 males, mean age 30 years), 14 were noted to have a decrease in mean arterial blood pressure (MAP) when sodium intake was increased from 10 to 100 mmol/d. The percentage response of plasma renin activity was greater in these patients than in those with an increase in MAP (-55.4 +/- 5.4 v -33.6 +/- 6.9, P = .018). Overall, the response of MAP was directly correlated to the percentage response of plasma renin activity (r = .549, P = .005), and inversely related to the change in serum calcium concentration (corrected for changes in serum albumin) (r = -.547, P = .005). No intercorrelation between the changes in plasma renin activity and serum calcium concentration was detected. The blood pressure response to increased sodium intake in high renin hypertension would appear to be divergent and related not only to the suppression of plasma renin activity, but also to changes in circulating calcium.
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PMID:Blood pressure and serum calcium responses to altered sodium intake in high renin hypertension. 264 17


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