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)

Angiotensin II (AII) and aldosterone (Aldo) in plasma, blood pressure (BP) and urinary excretion of sodium were studied before, during and in two periods after intravenous sodium loading with 500 ml of sodium chloride solution (50 g/l) in 11 normotensive and 10 hypertensive patients with histologically verified chronic glomerulonephritis and creatinine clearance in the range from 11 to 167 ml/min, and in 10 normotensive control subjects. The absolute increase of sodium excretion during loading was higher in the patients grouped together and in the hypertensives alone, but not in the normotensive patients when compared with the control subjects. No correlation was found between sodium excretion and control mean BP or change in mean BP during loading. AII and Aldo were suppressed during loading in both patients and control subjects. In the patients but not in the control subjects the increase of sodium excretion correlated positively with pre-infusion value of AII and negatively with change in AII during the sodium loading. No correlation was found between sodium excretion and Aldo and changes of Aldo. In conclusion, the results might suggest that the renin-angiotensin system is involved in the regulation of exaggerated natriuresis in chronic glomerulonephritis.
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PMID:Renin-angiotensin-aldosterone system in exaggerated natriuresis of chronic glomerulonephritis. 652 15

The effects of indomethacin on plasma renin activity (PRA), plasma and urine aldosterone levels and on renal function were studied in 37 patients with chronic glomerulonephritis (GN). Indomethacin produced a significant decrease in PRA, in plasma and urinary aldosterone levels and an increase in serum potassium levels. In 4 patients indomethacin induced the clinical syndrome of hyporeninemic hypoaldosteronism with hyperkalemia, which developed during the first weeks of treatment, persisted during treatment and disappeared without any additional drugs when indomethacin was stopped. In 14 patients with chronic GN, indomethacin caused a decrease in glomerular filtration rate (GRF). Their pretreatment PRA was significantly higher than that of patients with unchanged or increased GFR and most of them had prominent sclerotic changes on biopsy. Indomethacin considerably depressed diuresis and urinary sodium excretion. The antidiuretic and antinatriuretic effects of indomethacin were more pronounced in patients with the nephrotic syndrome. The results suggest that indomethacin exerts an effect on the renin-aldosterone axis, may be a cause of drug-induced hyporeninemic hypoaldosteronism and may cause a decrease in GFR in patients with high PRA.
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PMID:Effects of indomethacin on the renal function and renin-aldosterone system in chronic glomerulonephritis. 675 52

A woman, now 28 years old, was diagnosed 6 years ago as chronic glomerulonephritis by renal biopsy. From August 15, 1975 she complained of nausea, loss of appetite and weight (about 7 kg within 2 weeks). Severe hypertension (200/130 mmHg), hyponatremia (123 mEq/liter), anemia, elevated plasma renin activity (PRA), advanced azotemia, and eye ground changes of KW-II were found. Dialysis treatment was started on September 2, 1975. From November 1975 massive amounts of sodium (5,000 mEq or more monthly) and water (26 liters or more monthly) were removed by the dialysis. These intensive dialyses resulted in an elevated PRA with recurrence of severe hypertension. At the end of March 1976 she became almost blind with retinopathy of KW-IV. Potent hypotensive drugs including beta-blockers were administered, but no improvements were obtained. On March 31, 1976 nephrectomy was performed to save her life. Marked hyalinization of glomeruli and heavy thickening of intima in interlobular arteries were found in the removed kidneys. Renal artery stenosis was not recognized either macroscopically or histologically. In this patient, the amount of sodium removed by the dialysis was dependent on her diastolic blood pressure and sodium concentration of the dialysis. It may be concluded that too enthusiastic dialysis may develop malignant hypertension due to excessive renin release.
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PMID:Development of malignant hypertension in patients with uremia under hemodialysis: a case report and discussions on its etiology. 703 89

In twelve hypertensive patients with end-stage renal disease (ESRD) due to chronic glomerulonephritis (CGN), the mechanisms of renin and aldosterone regulation were studied by exogenously infused angiotensin II, captopril, and upright posture. The results were compared to those obtained in ten patients with unilateral renovascular hypertension (RVH), eleven patients with essential hypertension (EH), and in eleven normal subjects (NS). Exogenously infused angiotensin II (5.0 ng/kg/min) failed to decrease the plasma renin activity (PRA) in the ESRD group but significantly decreased the PRA in the RVH, EH, and NS groups. The plasma aldosterone concentration (PAC) in the ESRD group and in the other control groups significantly increased after the addition of exogenous angiotensin II. An oral dose of 50 mg of captopril failed to increase the PRA in the ESRD group. However, it significantly raised the PRA in the RVH, EH, and NS groups. The plasma aldosterone concentration was significantly reduced by captopril in the ESRD group, and similar results were obtained in the other three groups. The ratio between the PRA before and after being in an upright posture for 4 hours in the ESRD group was lower than that in the three other groups. Meanwhile, there was no difference in the PAC ratio between the ESRD group and the control groups. Thus, we conclude that, in hypertensive patients with ESRD due to CGN, PRA regulation is different from that in the other three groups, although there were no differences in the regulation of the PAC among the four groups, suggesting that renin production in the ESRD group is somewhat autonomous.
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PMID:The impaired control of plasma renin activity in hypertensive patients with end-stage renal disease due to chronic glomerulonephritis. 785 Oct 31

To determine whether renal reserve capacity was preserved in patients with chronic glomerulonephritis with well-preserved kidney function, and how sodium was handled in proximal and distal tubules, 13 healthy control subjects and 13 patients with biopsy-verified chronic glomerulonephritis were studied before and during a continuous 120-min amino-acid infusion. Glomerular filtration rate (GFR), renal plasma flow (RPF), and tubular function evaluated by the lithium clearance method, were determined during six clearance periods of 30 min each. Plasma concentrations of angiotensin II, atrial natriuretic peptide (ANP), aldosterone, arginine vasopressin (AVP), glucagon, amino acid and serum osmolality were determined before, 60, and 120 min after infusion. GFR and RPF increased about 10% in both groups; filtration fraction (FF) was unchanged. Proximal tubular reabsorption of sodium and water decreased, and distal tubular reabsorption of sodium and water increased, and thus the net excretion of sodium and water was unchanged. Angiotensin II and aldosterone were reduced in control subjects, but not in the patients. ANP and glucagon increased equally in both groups. Most amino acids increased two- or threefold. It is concluded that renal reserve capacity and glomerulotubular balance are intact in patients with chronic glomerulonephritis with well-preserved renal function, but there is an abnormal lack of suppression of the renin-angiotensin-aldosterone system in response to an amino acid infusion in these patients.
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PMID:Renal haemodynamic changes, renal tubular function, sodium and water homeostatic hormones in patients with chronic glomerulonephritis and in healthy humans after intravenous infusion of amino acids. 809 Mar 30

The authors examined 150 patients with pronounced arterial hypertension: 73 with essential hypertension, 42 with chronic glomerulonephritis, 26 with chronic pyelonephritis and 10 with diabetic glomerulosclerosis. In addition to conventional tests, measurements were made of renin activity, levels of plasma aldosterone and hydrocortisone, IgA, IgG, IgM, CIC. A significant rise in concentrations of aldosterone, hydrocortisone against a significant fall in those of plasma renin were registered in all the patients irrespective of the disease. Significant differences between the groups by the renin profile, aldosterone and hydrocortisone levels were absent. It is suggested that changes in the hormonal spectrum and immunological indices are independent of renal affections in hypertension, while involvement of renin-angiotensin-aldosterone system in hypertension stabilization has no nosological specificity. The pattern of the immunity shifts evidences for their important pathogenetic role in maintenance and progression of arterial hypertension.
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PMID:[Changes of the renin-angiotensin-aldosterone system and immunologic parameters in essential and symptomatic arterial hypertension]. 814 96

The antiproteinuric effect of the angiotensin-I-converting enzyme inhibitor, captopril, was studied in 14 patients (10 men and 4 women, age range of 24 to 60 years) with chronic glomerulonephritis in whom IgA nephritis had been confirmed by renal biopsy. Eight of the 14 patients had received antihypertensive drugs such as calcium channel blockers, diuretics or beta-blockers. Captopril was added to these regimens at 25 mg twice daily in 3 patients, and 37.5 mg in 11 patients. Proteinuria decreased from 2.55 +/- 0.48 g/day to 1.58 +/- 0.35 g/day within three months after the start of administration. In 4 patients (28.6%), the extent of reduction was over 50%, and in 8 patients (57.1%), over 25%. Blood pressure, creatinine clearance and serum creatinine were not changed significantly. There was a positive linear correlation between the extent of reduction of proteinuria and the increase in plasma renin activity (r = 0.93, p < 0.001). We conclude that captopril reduces proteinuria in some patients with IgA nephritis whose plasma renin activity responds to the drug.
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PMID:Effect of the angiotensin converting enzyme inhibitor, captopril, on proteinuria in chronic glomerular disease. 825 7

The effect of two angiotensin-converting enzyme (ACE) inhibitors, lisinopril and captopril, on proteinuria and renal haemodynamics was investigated in 11 hypertensives (9 men, 2 women; mean age 46 +/- 16 years) with proteinuria (> 1.5 g/24 h) due to chronic glomerulonephritis and impaired renal function (glomerular filtration rate < 75 ml/min). In a randomized and double-blind cross-over trial the patients received, each time for six weeks, either lisinopril (5 mg/d, sometimes increased to 10 mg/d after 3 weeks) or captopril (twice daily 12.5 mg, sometimes increased to twice 25 mg after 3 weeks). Initially and between the individual treatment phases they were on a placebo phase for 4 weeks. The following were measured: protein excretion, including fractional clearance of albumin and IgG, plasma-renin activity and renal haemodynamics. Protein excretion was not significantly reduced by either drug (placebo: 7.1 +/- 4.0 g/d; lisinopril: 5.1 +/- 2.8 g/d; captopril: 5.4 +/- 3.0 g/d). Albumin excretion and fractional albumin clearance were significantly decreased only by lisinopril (P < 0.05), not by captopril. Plasma-renin activity was increased more by lisinopril than captopril (Placebo: 1.0 +/- 0.9 ng/ml.h; lisinopril: 5.2 +/- 2.8 ng/ml.h [P < 0.05]; captopril: 1.8 +/- 1.3 ng/ml.h [P < 0.05]). The renal haemodynamics was only slightly influenced by either drug, but captopril significantly decreased the filtration fraction in the presence of chronic glomerulonephritis and renal failure. - Resulting from their influence on the renin-angiotensin-aldosterone system, ACE inhibitors have, in addition to their known action on renal haemodynamics, an independent effect on the loading barrier of the basal membrane of the kidney.
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PMID:[The effect of angiotensin-converting enzyme inhibitors on proteinuria in chronic glomerulonephritis]. 829 27

To determine the changes of the glucose-induced renin-angiotensin-aldosterone system in chronic renal disease, a standard oral glucose loading test (75g) was performed in patients with chronic glomerulonephritis (CGN) (n = 12) and compared with control subjects (10). Glucose loading resulted in a significant decrease of serum aldosterone as well as increases of blood glucose and insulin similarly in both CGN and C. However, the suppression of aldosterone was statistically milder in CGN than in C (p < 0.05). In contrast, significant elevations of plasma renin activity were observed in CGN at 60 and 120 min, but not in C after glucose loading. Urinary sodium excretion after glucose ingestion was lower in CGN than in C. These data demonstrated that the glucose-induced renin-angiotensin-aldosterone system in patients with chronic renal disease differed from that in healthy subjects.
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PMID:Acute effects of oral glucose loading on the renin-angiotensin-aldosterone system in patients with chronic renal disease. 845 6

Intrarenal and extrarenal humoral factors have been proposed as mediators and modulators of the renal hyperemic response to amino acid infusion. Among the potential modulators, angiotensin II (AII) constitutes the most important candidate due to its critical role in the control of glomerular and tubular function. The modulatory effect of AII has been assessed by (1) measuring the changes in plasma renin activity (PRA)/AII during the normal hyperemic response, and (2) by assessing the levels of PRA/AII and the response to AII-suppressing agents in conditions with no vasodilatory response during amino acid infusion. Administration of a protein load in normal animals or humans does not modify PRA/AII. Absence of a vasodilatory response in various experimental conditions (nitric oxide blockade in normal rats, experimental models of hypertension, diabetes mellitus, chronic glomerulonephritis, cyclosporine administration) is characterized by a significant decrease in proximal tubular reabsorption during amino acid infusion. Converting enzyme inhibitors or AII receptor antagonist restore normal tubular function and the increase in glomerular filtration rate during amino acid infusion. Absence of a vasodilatory response is also associated with increases in kidney AII levels in some of these conditions. These results suggest that (1) AII modulates the amino acid-induced hyperemia through its inhibitory effect on proximal tubular reabsorption and activation of the tubuloglomerular feedback system, and (2) that the expression of the modulatory effect of AII may depend on the interaction between AII and other intrarenal systems like nitric oxide.
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PMID:Role of angiotensin in the regulation of renal response to proteins. 852 41


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