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)

This study was designed to evaluate the role of aldosterone, glomerular filtration and blood pressure on sodium excretion in renal disease. Sodium clearance (CNa), plasma aldosterone (PA), plasma renin activity (PRA), glomerular filtration rate (GF), paraaminohippurate clearance (CPAH) and blood pressure were measured simultaneously in 19 normal subjects, 38 patients with benign essential hypertension, 3 with renal artery stenosis, 48 with chronic glomerulonephritis, 20 with the nephrotic syndrome, 24 with tubulo-interstitial disease and 21 with a renal homograft. CNa was significantly depressed in patients with the nephrotic syndrome. Mean PA and PRA were increased in renal artery stenosis but within the normal range in other groups. CNa correlated inversely with PA in all groups but one (tubulo-interstitial disease). CNa correlated directly with GF in the nephrotic syndrome and with the mean blood pressure (mBP) in chronic glomerulonephritis and tubulo-interstitial disease. PA correlated directly with PRA and inversely with GF or CPAH in most groups. It is concluded that PA is an important determinant of the basal natriuresis in renal disease with the exception of tubulo-interstitial nephropathies. In the nephrotic syndrome sodium retention is largely determined by the interaction of PA and GF. In chronic nephropathies, but not in benign essential hypertension, the fractional sodium excretion is partly blood pressure-dependent. Impairment of renal function is often accompanied by a rise in PA.
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PMID:Interrelationships between sodium clearance, plasma aldosterone, plasma renin activity, renal hemodynamics and blood pressure in renal disease. 39 72

There are typical morphological indicators of tubular defects during the administration of ciclosporin A (CSA). Distal tubular function remains unclear although hyperkalemia is a common clinical feature in these patients. We performed renal function studies 3 months after renal transplantation on 35 patients (group 1) treated with CSA. The results were compared to those of a control group consisting of 15 patients transplanted earlier and treated with azathioprine (group 2). Only patients with stable renal function (creatinine less than or equal to 2.0 mg/dl) entered the investigation consisting of: inulin (In) clearance; p-aminohippuric acid (PAH) clearance; ammonium chloride loading; sodium sulfate loading, and sodium bicarbonate loading. Plasma renin activity and aldosterone were measured basally and after stimulation with 40 mg i.v. furosemide. Clearances of In and PAH were significantly impaired during the administration of CSA. Group 1: CIn 73.3 +/- 8.7 ml/min/1.73 m2 (p less than 0.01), CPAH 263 +/- 58.3 ml/min/1.73 m2 (p less than 0.01); group 2: CIn 89.6 +/- 19.1 ml/min/1.73 m2, CPAH 338.7 +/- 63.5 ml/min/1.73 m2. Incomplete distal tubular acidosis could be demonstrated in 8 patients from group 1 but none of group 2. Hyporeninemic hypoaldosteronism could be demonstrated in 4 patients during the administration of CSA. CSA in therapeutic doses significantly impairs renal perfusion, glomerular filtration, distal acidification and the renin-aldosterone axis.
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PMID:Influence of ciclosporin A on renal tubular function after kidney transplantation. 165 70

The relations between renal hemodynamics (Inutest, CPAH) and sodium excretion were studied in 7 nondiabetics in whom a similar expansion was induced (1) with a 3-hour 5% glucose infusion and (2) with a 0.9% saline load. With both infusions the body weight increased, hematocrit fell, and the plasma renin activity was suppressed. During glucose infusion, blood glucose rose from 3.9 mmol/l to a plateau of around 13 mmol/l; glycosuria was absent during the 1st h, then appeared and stabilized during the following 2h. Glucose infusion caused a progressive increase in glomerular filtration rate and in renal blood flow in both absence and presence of glycosuria, without significant changes in sodium excretion despite volume expansion and increase of filtered sodium load. When saline was infused, there was a sustained increase of fractional sodium excretion, and no hemodynamic modifications were observed. We suggest that a primary glucose-induced metabolic stimulation of sodium reabsorption may play a role in the genesis of glucose-induced hyperfiltration.
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PMID:Sodium excretion and hyperfiltration during glucose infusion in man. 219 Apr 66

We demonstrated that potassium depletion significantly increased gentamicin nephrotoxicity in Sprague-Dawley rats (100 mg X kg-1 X day-1). To determine whether this enhanced toxicity was mediated by renin secretion, we evaluated the effect of a converting enzyme inhibitor in this model. When we administered the combination of captopril (100 mg X kg-1 X day-1) and gentamicin in potassium-depleted rats, we observed a surprising and significant adverse effect of this combination on the clearances of inulin (CIn) and PAH (CPAH) and renal blood flow (RBF). Pretreatment with indomethacin significantly improved CIn and CPAH, and potassium repletion abolished this effect entirely. In potassium-depleted animals that received both gentamicin and captopril, the intra-arterial administration of imidazole, a thromboxane synthetase inhibitor, significantly reduced urinary TXB2 excretion and significantly improved RBF and CIn in vivo. In the same group of animals, administration of the kallikrein antagonist aprotinin also significantly increased both RBF and CIn. To measure total renal thromboxane B2 production (TXB2), we perfused kidneys ex vivo with cell-free perfusate. Three groups of animals were studied: potassium-repleted control animals, potassium-depleted control animals, and potassium-depleted animals treated with gentamicin alone, captopril alone, or the combination of gentamicin and captopril. We measured TXB2 in renal venous effluent by radioimmunoassay. Ex vivo perfused kidneys from potassium-depleted control animals produced significantly more TXB2 than potassium-repleted controls. Kidneys from potassium-depleted animals that received both gentamicin and captopril produced significantly greater amounts of TXB2 than did kidneys from potassium-depleted animals treated with captopril alone, gentamicin alone, or control potassium-depleted kidneys. The administration of imidazole ex vivo at a rate equivalent to in vivo administration (10 microM/min) reduced TXB2 production by potassium-depleted kidneys that received the combination of gentamicin and captopril to that of potassium-repleted control kidneys. These results suggest that the deleterious effect of captopril in potassium-depleted rats that received gentamicin is due at least in part to kinin-stimulated renal TXB2 production.
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PMID:Captopril enhances aminoglycoside nephrotoxicity in potassium-depleted rats. 242 31

In order to evaluate the possible role of vasoactive hormones in the mechanism of exaggerated sodium loss due to reduced renal mass we measured plasma concentration of atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA), plasma noradrenaline, and dopamine, in 12 children with advanced chronic renal failure (mean CIn 17.8 +/- 2.6, mean +/- SEM, CPAH 93.5 +/- 17 ml/min per 1.73 m2, FENa 7.0 +/- 0.95%). No patient had clinical signs of volume overload. Plasma concentrations of ANP were not significantly different from those of healthy age-matched controls (29.2 +/- 7.2 vs 23.2 +/- 3.1 fmol/ml) and did not correlate with urinary sodium excretion. Plasma concentrations of aldosterone, PRA and noradrenaline, were also within the physiological range, while plasma dopamine levels were elevated (260 +/- 36 vs 98 +/- 11 pg/ml, less than 0.001). Our data do not support the notion that ANP or the renin-aldosterone axis play a major role in the adaptation of remaining nephrons to maintain long-term sodium balance in normotensive children with chronic renal failure.
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PMID:Atrial natriuretic peptide and sodium homeostasis in chronic renal failure. 253 71

The acute effects of bisoprolol 10 mg i.v., a new beta1-selective adrenoceptor antagonist, on heart rate, mean blood pressure (mBP), glomerular filtration rate (GFR), para-aminohippuric acid clearance (CPAH), sodium clearance, urine volume and plasma renin activity (PRA), were studied in 6 patients with essential hypertension. Heart rate decreased by 23%, mBP remained unchanged, and GFR decreased by 14% and CPAH by 23%. PRA was depressed on average by 25%. Urine volume and sodium clearance also declined by 9 and 13%, respectively, but the changes were not statistically significant. The fall in heart rate was significantly correlated with that in GFR and CPAH. Changes in GFR were correlated significantly with those in CPAH. The acute changes in renal function induced by bisoprolol are considered to be due to a reduction in cardiac output and increased systemic vascular resistance.
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PMID:Acute changes in renal function induced by bisoprolol, a new cardioselective beta-blocking agent. 287 82

Treatment of animal and human plasmas with pepsin yielded large quantities of immunoreactive methionine5-enkephalin (i-met-ENK). The concentrations measured after pepsin treatment were 0.1-0.5 microM, about 1000 times the normal circulating level of i-met-ENK (0.03-0.3 nM). The reaction was shown to be time and pH dependent and to involve the action of pepsin on a protein(s) of about 65,000 mol wt. Pepsin-generated i-met-ENK from rat plasma gave three major peaks during reverse phase HPLC, one of which (approximately 25% of the total) coeluted with methionine5-enkephalin sulfoxide and also completed in a radioreceptor assay for opiate-related substances. In addition, this material produced met-ENK-like effects on vascular permeability in rat skin and inhibited electrically induced contractions of the isolated guinea pig ileum in a naloxone-sensitive manner. The plasma substrate(s) that yielded i-met-ENK was distinguished from adrenal proenkephalins, since partially purified plasma substrate(s) did not liberate i-met-ENK upon digestion with trypsin and carboxypeptidase B. Although it is possible that these peptides differ from met-ENK in amino acid sequence, the results presented here suggest that met-ENK-related substances might be formed physiologically by the action of a pepsin-related processing enzyme(s) on plasma substrate(s). Such a mechanism would be analogous to that used in the renin-angiotensin system.
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PMID:Plasma protein(s) yields met-enkephalin-related peptides in near-micromolar concentrations when treated with pepsin. 309 94

Treatment of mammalian plasmas with pepsin yielded extraordinary quantities of immunoreactive neurotensin (iNT) and methionine5-enkephalin (iENK). The concentrations measured after pepsin-treatment (iNT, 1-5 microM and iENK, 0.1-0.5 microM) were 1-100 thousand times the normal circulating levels of these peptides. The reactions were shown to be time, temperature and pH dependent and to involve the action of pepsin on albumin-like proteins (Mr, ca, 65,000). Pepsin-generated iNT from rat plasma differed from NT since it reacted only with C-terminal directed antisera and eluted earlier than NT during HPLC on mu-Bondapak C-18. Partially purified iNT was active in two bioassays for NT, one which senses changes in vascular permeability to protein after intradermal injection into rats and another which measures release of histamine from isolated rat mast cells. Other biologic activities generated by pepsin-treating plasma included effects on systemic blood pressure in rats and on the contractility of the isolated guinea pig ileum. Some of these, however, were attributable to the formation of angiotensin- and bradykinin-related peptides. Pepsin-generated iENK gave three major peaks during HPLC, one of which (ca, 25%) co-eluted with oxidized ENK and also registered in a radioreceptor assay for opiate-related substances. In addition, this material produced ENK-like effects on the isolated guinea pig ileum and on vascular permeability in rat skin. The precursor-like protein(s) for iENK were distinguished from adrenal proenkephalins since it did not liberate iENK upon digestion with trypsin and carboxypeptidase B. Since pepsin can mimic renin these results suggest the existence of systems in blood (analogous to the renin/angiotensin system) for the generation of biologically active NT- and ENK-related peptides and they also raise the question as to whether other neuropeptides might be found circulating in precursor form(s).
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PMID:Generation of immunoreactive neurotensin(s) and enkephalin(s) by pepsin-treatment of plasma. 310 14

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.
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PMID:Four methods to recruit renal functional reserve. 311 62

Increasing doses of prostaglandin E2 (PGE2) (5, 10, 20, 40, 60 ng/kg/min) were infused in 7 normal volunteers before and after angiotensin II synthesis inhibition by captopril (100 mg by mouth). PGE2 infusion alone did not alter blood pressure, while it increased the urinary excretion of both epinephrine and norepinephrine, enhanced p-aminohyppuric clearance (CPAH), inulin clearance (CIn), sodium and water excretion and decreased urinary osmolality. No changes of CIn, CPAH and catecholamines were observed after captopril alone, whilst there was a significant increase in urine output and sodium excretion and a decrease in urinary osmolality. In the presence of captopril, the infusion of PGE2 caused a significant fall in blood pressure and CIn, enhanced epinephrine excretion and sodium excretion, while it did not significantly reduce CPAH. Our findings suggest that an intact renin-angiotensin system is necessary to maintain GFR during PGE2 infusion.
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PMID:Effects of PGE2 infusion on renal function in normal man before and after angiotensin II inhibition by captopril. 333 74


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