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 effects of heparin-induced aldosterone deficiency on renal sodium and potassium transport and renal function were studied in 65 patients with chronic glomerulonephritis and initial hyperaldosteronism. Heparin-induced aldosterone deficiency resulted in increased diuresis, in natriuresis due to decreased sodium reabsorption in the distal nephron, in a fall in serum sodium and an increase in serum potassium concentration. A transient reduction in potassium excretion occurred during the 2-4 days of heparin treatment. In patients with chronic glomerulonephritis and a compromised renin-angiotensin-aldosterone system, heparin may cause drug-induced selective hypoaldosteronism. The suppressive effect of heparin on aldosterone production was partially compensated for by increasing plasma renin activity. Heparin-induced aldosterone deficiency did not change glomerular filtration rate in patients without renal failure. In those with chronic sclerosing glomerulonephritis and a glomerular filtration rate less than 35 ml/min, heparin caused a further decrease in renal function.
Nephrol Dial Transplant 1987
PMID:Effects of heparin-induced aldosterone deficiency on renal function in patients with chronic glomerulonephritis. 311 60

The acute changes in creatinine clearance (Ccr) in response to intravenous amino acid infusion and to oral meat and milk protein meals were studied in seven healthy control subjects (Acute study). Para-aminohippurate clearance (CPAH), Ccr, inulin clearance (Cin), and plasma renin activity (PRA) were measured in seven different healthy control subjects following 1 week of low-protein diet, 0.7 g/kg per day, and again after one week of high-protein diet, 2.0 g/kg per day (Chronic study). In the acute study Ccr increased to a similar extent with each of the three stimuli, 20.1 +/- 6.2% (SD), 12.6 +/- 6.2% (SD) and 19 +/- 6.2% (SD) with amino acid infusion, 80-g meat protein and 80-g milk protein meals respectively. In the chronic study Ccr was 21%, Cin 26%, CPAH 8%, and filtration factor (FF) 14% greater during the high-protein diet than the low-protein diet, while PRA was increased by 43% on the high-protein diet. We conclude that an 80-g protein oral meal is probably sufficient to elicit the maximum acute increase in Ccr, since all three acute responses were similar, and similar in degree, to those previously reported, and may therefore be of value in measuring maximal filtration capacity. In contrast to one previous report, meat and milk proteins induced similar changes in Ccr. Thus milk protein cannot be regarded as a dietary substitute for meat in any diet designed to reduce glomerular hyperfiltration. Renin may play a part in the increase in glomerular filtration rate through the action of angiotensin II on the efferent arteriole, increasing filtration fraction.
Nephrol Dial Transplant 1987
PMID:Four methods to recruit renal functional reserve. 311 62

The influence of different vasoactive substances on the evolution of HgCl2-induced acute renal failure (ARF) was evaluated in the dog. HgCl2 alone caused a progressive fall in both glomerular filtration (GFR) and renal blood flow (RBF) during the first 3 h of the mercury administration (delta after 3 h: -44% and -39%) and provoked a concomitant stimulation of the renin-angiotensin (RAS) and thromboxane systems. The administration of the thromboxane inhibitor dazoxiben (2 mg/kg i.v. every 2 h) adequately inhibited the activation of the thromboxane system after HgCl2, but could not prevent the fall in GFR and RBF. The continuous intrarenal administration of the Ca2+ entry blocker verapamil (0.005 mg/kg per min) into the left kidney resulted in the prevention of the postmercurial fall in GFR and RBF at the perfusion site. This beneficial effect was immediately lost when the verapamil administration was stopped. Finally, the administration of the converting enzyme inhibitor captopril (300 micrograms/kg every 2 h) resulted in an effective inhibition of the renin-angiotensin system, the prevention of the postmercurial fall in RBF, and the partial attenuation of the fall in GFR. This beneficial effect was immediately lost after the intravenous administration of indomethacin (2 mg/kg). These results indicate that the fall in GFR after HgCl2 can be prevented by vasoactive agents such as captopril and verapamil and point at least in part to a pathophysiological role of the renin-angiotensin system or of an alteration in the equilibrium between renin-angiotensin and prostaglandins. The thromboxane system is seemingly of no major importance.
Nephrol Dial Transplant 1987
PMID:Influence of vasoactive substances on early toxic acute renal failure in the dog. 312 11

The hormones of the renin angiotensin aldosterone system were measured during regular haemodialysis with acetate or bicarbonate at dialysate sodium concentrations of 135, 140, 145, and 150 mmol/l. Plasma renin activity and aldosterone concentration were higher during acetate haemodialysis than during bicarbonate haemodialysis. At lower dialysate sodium concentrations, plasma renin activity (acetate dialysis and bicarbonate dialysis) and aldosterone concentration (only acetate dialysis) were higher than they were at higher dialysate sodium concentrations. Plasma renin activity increased during acetate dialysis, but did not change during bicarbonate dialysis. Aldosterone and potassium concentrations were positively correlated. Aldosterone decreased during haemodialysis (increase to predialysis values at the end of haemodialysis (4 h) at lower dialysate sodium concentrations). It is concluded that the renin angiotensin aldosterone system is activated more during acetate dialysis than during bicarbonate dialysis. Aldosterone concentrations seem to be related more closely to serum potassium than to renin-angiotensin-aldosterone system and to serum sodium intradialytically.
Nephrol Dial Transplant 1987
PMID:The renin-angiotensin-aldosterone system during haemodialysis with acetate or bicarbonate at different dialysate sodium concentrations. 312 54

Plasma renin activity and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and four prostaglandins (PGE2, PGF2 alpha, 6 keto PFG1 alpha and TXB2) in 23 patients with pregnancy induced hypertension (17 with permanent PIH and six with labile PIH, since in these latter their hypertension was controlled only by home bed rest) and in 16 normotensive pregnant women at the same stage of gestation (31 +/- 3 weeks). PRA was lower in permanent PIH than in controls and in labile PIH. No difference between the three groups was observed for plasma aldosterone and the urinary excretion of kallikrein and of the prostaglandins except that TXB2 was higher in labile PIH than in permanent PIH. Correlation studies of kallikrein disclosed correlations with most prostaglandin excretions, explained by the physiological stimulation of phospholipase A2 by kallidin. Correlation studies of PRA disclosed unexpected negative correlation with PGE2 and 6 keto PGF1 alpha in the permanent PIH group. In conclusion, labile PIH has a different biological profile than permanent PIH since they have higher PRA and higher TXB2 excretion, an association which suggests a more pronounced ureteral compression by the gravid uterus in this group. Permanent PIH has a disregulation of the renin angiotensin-prostacyclin loop since PRA and 6 keto PGF1 are negatively correlated. This suggests the role of an independent vasopressive substance which would stimulate PGI2 and suppress renin secretion.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Renin angiotensin aldosterone system, urinary prostaglandins and kallikrein in pregnancy induced hypertension. Evidence for a disregulation of the renin-angiotensin-prostacyclin loop. 384 87

The renin-angiotensin-aldosterone system and the acidification capacity of the renal tubule were studied in 13 diabetic patients with chronic renal failure. As a whole, the group showed hyporeninaemic hypoaldosteronism (HH). Studied alone, 12 of the 13 patients presented the requirements for HH. This group showed hypercholaemic hyperkalaemic metabolic acidosis with a disturbance in renal acidification which may be classified as Type IV renal tubular acidosis. The results of this group were compared to those of another two groups; one of diabetic patients without chronic renal failure and the other with chronic renal failure (C Cr less than 40ml/min); both were seen to show different behaviour to that of the group affected by the two processes.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Plasma renin activity, plasma aldosterone and distal urinary acidification in diabetics with chronic renal failure. 399 78

In order to study the effect of epinephrine on potassium (K) metabolism, an epinephrine infusion (0.1 micrograms/kg/min for 30 min) was carried out in 12 essentially anuric and usually hyperkalaemic haemodialysis patients, 72 hr post-dialysis. Two groups emerged, group I (five patients) serum K decreased at least 0.75 mEq/L (from 6.6 +/- 0.2 to 5.4 +/- 0.1 mEq/L) and there were increases in heart rate, serum glucose and insulin values, group II (seven patients), serum K did not decrease and heart rate remained unchanged, but serum glucose and insulin increased slightly. Plasma renin, aldosterone and arterial pH did not change in either group. Propranolol blocked the epinephrine induced decrease in serum K in group I patients. Patients from group II had higher pre-infusion endogenous epinephrine concentrations than patients from group I. In haemodialysis patients beta adrenergic stimulation enhances extrarenal K disposal but about 50 per cent of patients fail to respond, perhaps because of receptor occupancy due to higher endogenous epinephrine concentrations.
Proc Eur Dial Transplant Assoc 1983
PMID:Beta adrenergic modulation of extrarenal potassium disposal in terminal uraemia. 613 35

The role of prorenin in relation to beta-blockade has received little attention. We have studied both active renin and prorenin before and during treatment of hypertension with either nadolol or metoprolol in 44 patients. The ratio of active renin to prorenin before treatment was the best predictor of response; the fall in active renin with treatment did not correlate with the fall in blood pressure, whereas prorenin showed an inverse correlation. We suggest that plasma prorenin is an important indicator of the renin status in hypertensive patients.
Proc Eur Dial Transplant Assoc 1983
PMID:Prorenin and beta-blockade in hypertension. 614 Jun 78

In order to determine the molecular basis for the loss of catecholamine responsiveness in skeletal muscle in chronic azotemia, plasma and serum levels of catecholamines and other hormones whose mechanisms of action are associated in part with cyclic nucleotide mediation were assessed in 37 patients with chronic azotemia. Samples were obtained prior to and immediately following conventional hemodialysis. Plasma epinephrine and norepinephrine levels in patients predialysis were increased 50% and 25% respectively compared to control subjects. Levels of insulin, prolactin, aldosterone and renin were also in creased in azotemic patients prior to dialysis. Conventional hemodialysis reduced serum levels of growth hormone, but had no effect of the elevated levels of all other hormones found in patients predialysis. In particular, plasma epinephrine and norepinephrine levels were unaffected by hemodialysis. Despite these findings, hemodialysis did reduce to normal levels the elevated plasma levels of cyclic AMP and cyclic GMP observed in uremic subjects predialysis. These data are consistent with increased adrenergic outflow in patients with chronic azotemia, and suggest a mechanism of homologous desensitization of the catecholamine receptor adenylyl cyclase unit in chronic azotemia.
J Dial 1980
PMID:The effect of hemodialysis on levels of cyclic nucleotide-associated hormones in patients with chronic renal failure. 625 22

Vascular damage (VD), glomerular sclerosis (GS), renin (PRA) and blood pressure were assessed in 50 patients with Berger's nephropathy. GS was present in 5/15 patients without VD and affected more than 15 per cent of glomeruli in seven patients with minimal VD. Nine out of 19 patients with GS were normotensive. VD was present in 35 patients: 16 were hypertensive and 19 normotensive. Therefore hypertension is not the only mechanism responsible for VD. In the seven normotensive patients with high PRA, GS was not present while VD was absent or minimal.
Proc Eur Dial Transplant Assoc 1983
PMID:Berger's nephropathy: relationship between histological pattern, blood pressure and renin. 634 61


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