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)

To investigate the origin, the mechanisms of regulation and the possible biological significance of inactive renin we examined the effects of haemodialysis on plasma active and inactive (cryoactivatable) renin in four anephric and in 10 nephric patients. Before haemodialysis inactive renin was similar in anephric and in the majority of nephric patients; this suggests that the source of the inactive enzyme is predominantly extrarenal. In response to haemodialysis active renin rose significantly in nephric patients whereas inactive renin showed minor and inconsistent increments in both groups. These results indicate that the response of the inactive enzyme to haemodialysis is less than that of its active counterpart and is unaffected by the presence of the kidneys. Therefore, it appears unlikely that inactive renin represents a circulating precursor of active renin.
Proc Eur Dial Transplant Assoc 1983
PMID:Effects of haemodialysis on active and inactive renin in nephric and anephric patients. 636 56

In 39 healthy pregnant women and 45 women with mild or moderate late pregnancy toxaemia (LPT) the influence of head-out water immersion on blood pressure, the renin-aldosterone system, vasopressin and plasma osmolality was examined. Water immersion induced a prompt and marked fall in systolic and diastolic blood pressure, which was significantly higher in LPT women. Simultaneously a significant decrease of plasma renin activity, aldosterone and vasopressin was noted both in healthy and toxaemic pregnant women. In contrast to healthy pregnant women in LPT haemodilution was not observed in the early phase of water immersion.
Proc Eur Dial Transplant Assoc 1983
PMID:Influence of head-out water immersion on plasma renin activity, aldosterone, vasopressin and blood pressure in late pregnancy toxaemia. 636 58

The participation of renal prostaglandins in the nephrotic syndrome has been investigated by the measurement of the urinary excretion of prostaglandin E2 (PGE2), renal function and the renin-angiotensin-aldosterone system before, during and after the administration of indomethacin in a group of patients diagnosed as having chronic idiopathic glomerulonephritis with and without nephrotic syndrome. Our results indicate increased renal production of PGE2 in nephrotic patients. This contributes to the maintenance of renal function, probably by counteracting an activated renin-angiotensin system and could be accompanied by a simultaneous and deleterious enhancement of the degree of proteinuria. Nevertheless, the participation of angiotensin II in this last even cannot be excluded.
Proc Eur Dial Transplant Assoc 1983
PMID:Participation of renal prostaglandins in the nephrotic syndrome. 657 32

The possible vasodepressor role of the renal medulla was studied by chemical medullectomy (i.v. bromoethylamine hydrobromide) in rats. A significant increase in blood pressure (BP) was observed 10 weeks after injection which related to the increase in urinary volume and decrease in urinary prostaglandin E2 (PGE2) in medullectomised rats, but not to plasma renin concentration (PRC). Creatinine clearance was unchanged. The differences between control and medullary damaged rats were maintained over a wide range of sodium intakes although the patterns of response were similar in the two groups. The increase in BP observed following renal medullectomy is likely to be secondary to a reduction in interstitial cell function.
Proc Eur Dial Transplant Assoc 1983
PMID:Chemical renal medullectomy and experimental hypertension. 658 83

Conversion to alternate day prednisone therapy resulted in a reduction in blood pressure in hypertensive renal transplant recipients. Plasma renin activity was also reduced and may be connected with the fall in blood pressure. There was evidence of increased aldosterone activity, possibly mediated by ACTH, but there was no evidence that the fall in blood pressure was due to changes in sodium status.
Proc Eur Dial Transplant Assoc 1980
PMID:Alternate day steroids and blood pressure control after renal transplantation. 701 96

In seven splenectomised dogs a left renal vein-splenic vein anastomosis was performed and the right kidney removed. Eighteen to twenty-four months after portalisation of renal venous blood no significant alterations of liver function tests were found. Long-term diversion of renal venous blood into the liver was followed by a slight increase of creatinine and 25(OH)D3, a decrease of alpha-amino acid nitrogen in blood plasma and of plasma renin activity in peripheral blood, by symptoms of slight carbohydrate intolerance despite hyperinsulinaemia and a slight decrease of erythrocytosis. No influence of this procedure on plasma proteins, lipids, electrolytes, aldosterone and cortisol was observed. No morphological abnormalities in liver and kidney tissues were found.
Proc Eur Dial Transplant Assoc 1980
PMID:Metabolic effects of long-term diversion of renal venous blood into the portal system. 701 1

Systemic, humoral and renal responses to isotonic volume expansion (VE, 1800ml in 3 hours) were assessed in normal subjects before and during captopril administration (CEI). Captopril, which otherwise induced a decrease in pre-saline mean arterial pressure (MAP) unmasked the volume-dependence of MAP since during captopril administration MAP increased linearly during volume expansion (+18.7 +/- 3.8% at the end of VE). In addition, captopril prevented the fall in plasma aldosterone produced by VE but did not modify the natriuretic response to saline. These results demonstrate that circulating angiotensin II is not an important determinant of the natriuretic response to volume expansion in normal man. However, a role for intrarenal renin cannot be excluded.
Proc Eur Dial Transplant Assoc 1981
PMID:Effect of captopril on the systemic and renal responses to acute isotonic volume expansion in normal man. 703 74

Renin secretion may be modulated by nitric oxide (NO). We studied whether interleukin-1 beta (IL-1 beta) induces endogenous NO synthesis in mouse juxtaglomerular cells (JGC) in primary culture, and whether endogenous NO or NO applied exogenously via sodium nitroprusside (SNP) influences renin secretion. JGC seeded on culture plates were stimulated by IL-1 beta or by SNP. Cyclic guanosine 3,5'-monophosphate (cGMP) in the cell supernatant was determined as indicator for NO effects. Stimulation of JGC with IL-1 beta or SNP increased cGMP in the supernatant significantly. The NO synthase inhibitors NG-nitro-L-arginine or NG-monomethyl-L-arginine, or the NO scavenger oxyhaemoglobin prevented the IL-1 beta-induced increase of cGMP. The biological activity of NO was shown in a bioassay by the vasodilatory effect of the effluent from an IL-1 beta-stimulated JGC column on a precontracted rat aortic ring and was prevented by oxyhaemoglobin and methylene blue. Renin activity of JGC was detected in the culture supernatants and the cells. Spontaneous renin secretion into the cell supernatant was 26 +/- 1% of total activity. Melittin or forskolin concentration dependently increased renin secretion up to 90 +/- 2%. Incubation of JGC with IL-1 beta in the absence or presence of NO inhibitors did not alter spontaneous or stimulated renin secretion. SNP (30 microM) had a dual effect on renin secretion. After 1 h of incubation, it inhibited basal renin secretion, whilst it had a stimulatory effect after 20 h of incubation.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1995
PMID:Interleukin-1 beta induces the formation of nitric oxide in isolated juxtaglomerular cells: influence on renin secretion. 753 49

Systemic hypertension has been reported to develop, or to worsen, in 20-30% of patients treated with recombinant human erythropoietin (r-HuEPO) worldwide. The greatest increases in blood pressure affect day-time systolic and night-time diastolic blood pressure. Hypertension may develop in some patients as early as 2 weeks and in others as late as 4 months after the start of r-HuEPO treatment. In haemodialysis patients with systemic hypotension, r-HuEPO usually induces a 10% increase in blood pressure, with no significant change in the frequency of hypotensive episodes. Several risk factors for the development, or worsening, of hypertension after r-HuEPO therapy have been identified. They include the presence of pre-existing hypertension, rapid increase in haematocrit, a low baseline haematocrit before r-HuEPO administration, high doses and i.v. route of administration, the presence of native kidneys, a genetic predisposition to hypertension, and possibly a younger age. There are several potential mechanisms by which r-HuEPO therapy may increase blood pressure in haemodialysis patients. They include increased blood viscosity; the loss of hypoxic vasodilation; the activation of neurohumoral systems (catecholamines, the renin-angiotensin system); and especially a direct vascular effect. This last mechanism is supported by several data, and many factors may be involved in its pathogenesis (an increased cell calcium uptake; an imbalance in local vasoactive agents, with increased synthesis of ET-1; a mitogenic effect; and a platelet-dependent mechanism).
Nephrol Dial Transplant 1995
PMID:Erythropoietin and systemic hypertension. 764 10

The Han: SPRD Pkd rat mutant is an autosomal dominant rat model with incomplete penetration of polycystic renal transformation. Progressive renal failure occurs in heterozygous male animals. The mechanisms of progression have not been elucidated. To identify some pathogenetic factors involved we subjected male SPRD Pkd rats (and their non-affected littermates as controls) to uninephrectomy (UNX), castration or enalapril treatment. To assess progression S-urea at age 150 days was chosen as endpoint. (i) In uninephrectomized male Han: SPRD Pkd (n = 12 animals per group) S-urea at age 150 days was consistently above 300 mg/dl, while it was 245 mg/dl (191-290) in control Han: SPRD Pkd. (ii) In castrated male Han: SPRD median S urea at 150 days was 100 mg/dl (69-211) compared to sham-operated male Han: SPRD controls (245; 191-290). Castration did not, however, prevent accelerated progression after uninephrectomy. (iii) Enalapril (50 mg/l) in the drinking fluid did not significantly lower median systolic blood pressure (by plethysmography) in animals on 0.2% sodium diet (at 185 days 160 mmHg; 140-170 versus 170; 140-195 in non-enalapril controls), although circulating ACE was significantly inhibited (17 U; 11-33 versus 89; 52-108 in controls). S-urea at age 185 days was not significantly different in the 2 groups. In conclusion, the Han: SPRD Pkd model differs from human ADPKD to some extent. Uninephrectomy accelerates renal failure in the rat, but not in humans. On the other hand, in contrast to human ADPKD the renin system is suppressed in the rat model and ACE inhibition does not affect the course of renal failure.
Nephrol Dial Transplant 1994
PMID:Progression of renal failure in the Han: SPRD polycystic kidney rat. 770 56


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