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)

The effect of propranolol has been studied in two patients with chronic renal failure and hypertension which remained refractory despite the removal of excess sodium and water by dialysis. Measurements of plasma-renin, exchangeable sodium, and blood-volume demonstrated that in both patients hypertension was due to excess renin. The administration of propranolol was followed by a rapid fall in blood-pressure to normal, thereby obviating the need for bilateral nephrectomy. In both patients the fall in blood-pressure was accompanied by a striking fall in plasma-renin, and in one there was a highly significant association between plasma-renin activity and mean arterial pressure.
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PMID:Effect of beta-adrenergic blockade on plasma-renin activity and intractable hypertension in patients receiving regular dialysis treatment. 5 51

Captopril (SQ 14 225), an orally active inhibitor of angiotensin-converting enzyme, was given to 7 hypertensive patients with chronic renal failure whose plasma-creatinine ranged from 1.5--7.4 mg/dl; whose plasma-renin activity was normal; whose hypertension was not controlled by previous therapy consisting in 5 patients of three or more antihypertensive drugs; and whose blood-pressures averaged 176/111 +/- 11/3 mm Hg. Inhibition of converting enzyme by oral captopril, 200 mg twice daily, reduced blood-pressure to 156/100 +/- 9/5 mm Hg. 5 patients needed additional treatment by frusemide 40--250 mg/day orally. With this combined regimen the blood-pressure of all patients averaged 126/85 +/- 4/3 mm Hg after 8 +/- 2 weeks of captopril. The drug was well tolerated. These results suggest that inhibition of angiotensin-converting enzyme with or without sodium depletion is an efficient treatment for hypertension associated with chronic renal failure. It appears that although renin levels in patients with this condition may be "normal", they are inappropriate in relation to the subtle degree of sodium retention that occurs with this disorder.
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PMID:Innappropriate renin secretion unmasked by captopril (SQ 14 225) in hypertension of chronic renal failure. 8 Jun 34

The purpose of the present study was to examine the influence of different sodium loads on renin release in the hypertensive and normotensive state of chronic renal failure. Blood pressure (BP), plasma renin concentration (PRC) and exchangeable sodium (NaE) were measured in eighteen patients with advanced chronic renal failure, nine hypertensives and nine normotensives, and in seven normal subjects (a) 6 days after a fixed sodium intake of 10 mmol/day, and (b) 6 days after a fixed sodium intake of 150 mmol/day. Mean NaE was 14-19% higher in the hypertensives compared with the normotensives and values of NaE correlated significantly to values of mean BP. No significant differences were present in PRC between the groups of patients and controls on either of the sodium regimens and no correlation was found between BP and PRC. However, average decreases of PRC in the hypertensives on high sodium intake, 33-34%, were significantly lower than the corresponding values of 69-71% in the normotensive patients and controls, respectively. Furthermore, the percentage changes of PRC on high sodium intake correlated significantly to mean BP as well as to NaE. These results suggest that renin release is relatively unresponsive to different sodium intakes in hypertension following chronic renal failure. This alteration in renin release may contribute to the maintenance of hypertension in chronic renal failure, PRC being "inappropriately' increased in relationship to the sodium excess.
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PMID:The influence of different sodium loads on renin release in hypertensive and normotensive states of chronic renal failure. 14 27

The relationship between plasma potassium concentration and the renin-angiotensin-aldosterone system was evaluated in ten patients with chronic renal failure (creatinine clearance 10-56 ml/min). Under basal conditions and following various stimulation maneuvers, normokalemic patients demonstrated normal plasma renin and aldosterone levels. Five of six patients with hyperkalemia had diminished function of the renin-angiotensin-aldosterone system; their ability to conserve sodium during salt depletion was less than that of normokalemic patients. The data suggest that the maintenance of plasma potassium levels in these patients is dependent of the presence of a normally functioning renin-angiotensin-aldosterone system; aldosterone activity may be an important determinant of sodium conservation in patients with renal failure.
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PMID:Role of the renin-angiotensin-aldosterone system in the regulation of plasma potassium in chronic renal disease. 16 38

The antihypertensive effect of the orally active angiotensin-converting enzyme inhibitor captopril (SQ 14225) was assessed in 22 hypertensive patients of whom 17 were followed for periods ranging from 1 to 7 months. Of these, eight had essential hypertension, eight had renovascular hypertension, and six had hypertension associated with chronic renal failure. Blood pressure decreased markedly in all patients, including those with low renin levels. Nevertheless, the magnitude of blood pressure reduction correlated with the base-line plasma renin activity (r = 0.58, P less than 0.01). Increasing the dose of captopril from 25 to 200 mg did not enhance the amplitude of the antihypertensive effect but did increase its duration. Patients' blood pressure remained well controlled and free of side-effects with a maximal daily dose of up to 200 mg by mouth twice daily. Despite the blood pressure reduction, sodium excretion tended to increase, probably because of reduced aldosterone secretion. There was no evidence of orthostatic hypotension, and no escape from the antihypertensive effect was observed. These results indicate that chronic inhibition of the angiotensin-converting enzyme with an orally active compound offers a new, efficient, and well-tolerated approach to the treatment of hypertension.
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PMID:Oral angiotensin-converting enzyme inhibitor in long-term treatment of hypertensive patients. 21 89

Serum angiotensin converting enzyme activity was assayed by a spectrofluorometric method in 19 patients with chronic renal failure on long term hemodialysis and 19 control subjects. Converting enzyme activity was increased in 11 of 19 (58%) patients compared with the controls (p less than 0.005). There was no correlation between serum converting enzyme activity and plasma renin activity or blood pressure in the patients. Possible mechanisms responsible for the increased converting enzyme activity are discussed.
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PMID:Serum angiotensin converting enzyme activity in patients with chronic renal failure on long term hemodialysis. 21 70

The factors regulating aldosterone secretion in normals and in patients on chronic hemodialysis were studied by the determination of the circadian rhythm of plasma aldosterone, renin, cortisol, insulin, potassium, sodium, and glucose. Four normal volunteers and eight normotensive patients on regular dialysis treatment (RDT) were studied during prolonged recumbency on low sodium diet. A definite circadian rhythm for renin could not be demonstrated in RDT patients. The significant simple and multiple correlation coefficients found in normal subjects suggest that insulin participates in the regulation of aldosterone together with the other known factors: ACTH, renin, and potassium. In chronic renal failure, however, when basal conditions were maintained during prolonged recumbency, the correlations of insulin and renin with aldosterone were not found, suggesting that in this condition aldosterone secretion is controlled by ACTH and potassium. As a direct influence of insulin on aldosterone could not be demonstrated by multiple variance analysis, it seems that insulin is related to aldosterone indirectly through renin and/or potassium. The presence of significant correlations between insulin-potassium and potassium-aldosterone in RDT patients, without a significant insulin-aldosterone correlation, suggest that in the normals insulin participates in aldosterone regulation through renin secretion and not through potassium. A correlation between potassium and renin was not found in normals or in RDT patients.
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PMID:Presence of insulin-renin-aldosterone-potassium interrelationship in normal subjects, disrupted in chronic hemodialysis patients. 40 Jul 16

Plasma renin activity (P.R.A.) and plasma aldosterone (P.A.) were studied basally and after various stimuli in eight diabetic subjects with orthostatic hypotension and autonomic neuropathy. Five of them had chronic renal failure and proteinuria. On a diet containing 100 mEq Na/24 H, mean P.R.A. was 0,80 +/- 0,32 ng/ml/h in the supine position and 0,95 +/- 0,43 ng/ml/h in the upright position (N.S.); mean P.A. was 111 +/- 77 pg/ml in the supine position and 234 pg/ml in the upright position (p less than 0,01). On a diet containing 10 mEq Na/24 H, mean P.R.A. was 1,54 +/- 0,76 ng/ml/h in the supine position and 2,44 +/- 1,53 ng/ml/h in the upright position (N.S.). There was little stimulation of P. R. A. by low sodium intakes. After furosemide (n = 6), epinephrine + norepinephrine (n = 4) or diazoxide (n = 2), there was no stimulation of P.R.A. and P.A. Thus in diabetic patients with orthostatic hypotension and autonomic neuropathy basal values of P.R.A. and P.A. are in the normal range but there is dysregulation of renin-angiotensin-aldosterone system.
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PMID:[Orthostatic hypotension in complicated diabetes mellitus: study of the renin-angiotensin-aldosterone system (author's transl)]. 44 29

In a group of four young patients with stable chronic renal failure and hyperkalemia sodium restriction induced a remarkable increase in plasma renin activity (PRA) and plasma aldosterone (PA), a decrease in the elevated serum potassium (SK) and a rise in potassium excretion. During high sodium intake the levels of PRA and PA were lower than those found in the healthy control group suggesting that enhanced suppressibility of the renin-angiotensin-aldosterone system (RAAS) was the main cause of hyperkalemia. During sodium restriction despite a marked increase in PRA and PA levels poor correlations were found between these variables indicating disorganisation within the RAAS and probably a diminished role for renin-angiotensin in the regulation of aldosterone production in three hyperkalemic patients with chronic glomerulonephritis. On the other hand, in the same patients significant correlations were found between fluctuations of SK and PA on constant normal and low sodium diets supporting the concept of an (at least) equal role of potassium and RAAS in the acute regulation of PA. A prominent role for SK was found in an unusual hyperkalemic patient with interstitial nephritis when PRA was suppressed and the elevated SK showed a definite postural rise inducing dramatic increases in PA in the upright posture. Reversion of the postural SK rise masked again the governing role of SK.
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PMID:Regulations of plasma aldosterone in young hyperkalemic patients with stable chronic renal failure. 46 73

Forty-three patients suffering from hypertension of different origin (chronic renal failure, gout, or idiopathic) were treated with propranolol (121 +/- 12 mg q.d.) plus hydrochlorothiazide (50 mg q.d.) for 75 +/- 9 days. Blood pressure did not return to normal limits in 15 patients, who were continued on the same protocol plus 10 to 50 mg oxdralazine q.d. After an average of 68 +/- 35 days blood pressure fell from 180/110 mm Hg to 145/90 mm Hg without orthostatism, significant side effects, or changes in GFR. This combination seems particularly successful since propranolol will prevent the undesired rise in cardiac output due to oxdralazine as well as the activation of the renin-angiotensin axis due to diuretics. Thus, the antihypertensive properties of each agent will be enhanced by a reduction in side effects by the associated drug, resulting in optimal blood pressure control.
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PMID:Oxdralazine, a new peripheral vasodilator, combined with propranolol and hydrochlorothiazide: a rational approach to antihypertensive treatment. 53 72


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