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)

A closed loop closed batch dialysate delivery system was used to determine whether Na or K has an action on the renin-angiotensin system apart from volume changes. Twenty-eight patients on chronic haemodialysis were studied, 12 (group I) were normotensive and 16 (group II) had poorly controlled hypertension. Acute Na depletion or repletion (delta NA), AND K loss (delta K) were induced with or without net water loss. Net electrolyte and water movement across the dialysis membrane could be precisely quantitated.
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PMID:Effect of acute sodium or potassium depletion on plasma renin activity in haemodialysed patients. 99 Mar 87

The present experiments were performed to study the effect of chronic extracellular volume expansion on the magnitude of tubulo-glomerular feedback responses in the rat kidney. Extracellular volume expansion was achieved by giving isotonic saline as drinking water and by injecting DOCA in a dose of 2.5 mg/kg - day. When Ringer perfusion rate through the loop of Henle was elevated in control rats (receiving only saline as drinking water) stop flow pressure (SFP) fell by an average of 0.47 +/- 0.81 mm Hg (mean +/- S.D.) and 7.93 +/- 2.85 mm Hg at the flow rate steps of 0--15 nl/min and 15--40 nl/min respectively. SN-GFR was reduced by a mean of 1.3 +/- 0.97 nl/min (0--15 nl/min) and 10.3 +/- 2.45 nl/min (15--40 nl/min). In DOCA treated rats the mean reductions of SFP were 0.98 +/- 0.9 mmHg and 2.1 +/- 1.4 mmHg and of SN-GFR 0.06 +/- 1.8 nl/min and 1.94 +/- 2.3 nl/min. Thus, significantly smaller changes of both SFP and SN-GFR were found in DOCA treated animals when flow rate was elevated from 15--40 nl/min. Net loop NaCl absorption rates did not significantly differ between control and DOCA rats. Renin activity of 5 pooled microdissected glomeruli was 15.6 +/- 17.1 ng/hr-0.1 ml in control and 2.94 +/- 2.6 ng/hr-0.1 ml in DOCA treated rats (P less than 0.01). It is possible therefore that the reduced feedback reactivity in DOCA treated rats is related to the diminished juxtaglomerular renin activity.
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PMID:Impaired potency for feedback regulation of glomerular filtration rate in DOCA escaped rats. 117 14

Some measures of the efficacy of fluid resuscitation after hemorrhage are blood volume restitution (BVR) and attenuation of the neuroendocrine response. We compared the effectiveness of resuscitation with 0.9% NaCl and 3.0% NaCl in chronically prepared awake dogs after 30% hemorrhage. Each dog was bled on four occasions and resuscitated by four protocols: 1) full resuscitation (infusion to return and maintain mean arterial pressure (MAP) at control +/- 10 mm Hg) with 3.0% NaCl (HS); 2) full resuscitation with 0.9% NaCl (NS); 3) under-resuscitation with a volume of 0.9% NaCl equal to the subject's previous 3.0% NaCl requirement (SV); and 4) no fluid therapy (NR). Approximately three times more volume was needed to restore MAP with NS vs. HS, and thus the amount of Na administered was not different in these groups. Net volume balance was positive in the NS and SV groups but negative in the HS group due to marked saline diuresis. Net Na balance was positive in all three fluid-treated groups, but significantly higher in the HS group (p less than 0.01). MAP remained below baseline in the SV and NR groups (p less than 0.05). BVR exceeded 100% in NS and HS early in resuscitation, but BVR was not sustained in the HS group. Total plasma protein increased in all three fluid treated groups. Responses of all hormones were completely attenuated in the NS group. ACTH, cortisol, and AVP responses were promptly attenuated in the HS group, but remained greater than control. In the SV group, all hormone levels except renin returned to control values, but more slowly than the other groups. ACTH and cortisol correlated best with BVR; AVP, PRA, and aldosterone correlated with MAP restoration. In summary, resuscitation with either HS or NS can achieve similar MAP restoration. Hypertonic saline produces a more rapid increase in BVR and MAP, but the BVR improvement is transient. Resuscitation with HS incurs an intracellular water debt which is aggravated by a saline diuresis. Hormonal attenuation is linked either to BVR (ACTH, cortisol) or to MAP restoration (renin, AVP). Thus the optimal resuscitation regimen may consist of initial infusion of hypertonic saline followed by sufficient hypotonic solution to restore interstitial fluid volume and normal cellular hydration.
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PMID:Interaction of sodium and volume in fluid resuscitation after hemorrhage. 185 Apr 88

Renal function was evaluated in six patients with fetal alcohol syndrome (FAS) and eight control subjects before and after fluid restriction and acute acid loading. Baseline serum electrolytes, creatinine clearance, fractional sodium excretion, tubular reabsorption of phosphate, urine and blood pH and osmolalities, plasma renin activity, and plasma aldosterone level were normal in all subjects, but fractional potassium excretion (FEK) was lower in FAS patients than in control subjects (P less than 0.001). Despite equivalent plasma osmolalities (295 +/- 3 vs 293 +/- 2 mosmol/kg, P = 0.2), the maximum urinary osmolality after 12 h of water deprivation in patients with FAS was significantly lower compared with controls (560 +/- 107 vs 965 +/- 77 mosmol/kg; P less than 0.001) and increased to only 578 +/- 101 mosmol/kg after vasopressin administration. After ammonium chloride loading, minimum urine pH was significantly higher in patients than in controls (5.7 +/- 0.17 vs 4.81 +/- 0.19; P less than 0.001). Net acid excretion and FEK were also lower in patients than in controls (102 +/- 11 vs 139.6 +/- 11.3 microEq/min per 1.73 m2 and 23.5 +/- 1.3 vs 29 +/- 1.6%, respectively; P less than 0.001). The data indicate a subclinical renal tubular defect in urine concentration and acidification in patients with FAS.
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PMID:Renal tubular dysfunction in fetal alcohol syndrome. 220 81

1. Previous studies of endogenous atrial natriuretic peptide (ANP) in humans have examined changes in plasma levels, rather than regional secretion and clearance of the peptide. Using arterial and selective venous catheterization and sampling, and measurement of regional organ flow, we measured haemodynamics, cardiac secretion of ANP and renal clearance of ANP in six healthy volunteers at rest, on a normal sodium diet. 2. Salt restriction decreases plasma concentrations of ANP. We assessed the contribution of the heart and kidney to this decrease, by measuring cardiac secretion and renal clearance of ANP at the termination of a low salt diet. 3. Twenty-four hour urinary sodium excretion fell on the low salt diet from 163 to 29 mmol/day [standard error of the difference (SED)+/- 14, P less than 0.001]. Body weight decreased on salt restriction from 76.4 to 75.4 kg (SED +/- 0.33, P less than 0.05). Brachial mean arterial pressure fell by 6% (P less than 0.05), but right atrial pressure was unchanged. Renal vein plasma renin activity increased by 56% with sodium restriction (P less than 0.01), whereas arterial ANP concentrations fell by 39% (P less than 0.05). 4. Coronary sinus ANP levels fell from 417 to 268 pg/ml (SED +/- 74, P less than 0.05), whereas renal vein concentrations were unaltered. There was a 47% decrease in cardiac secretion of ANP in the low salt state (P less than 0.05). Net extraction of ANP across the kidney (about two-thirds) and renal clearance of ANP were unchanged on the low salt diet. Thus decreased plasma ANP with sodium restriction is due to reduced cardiac secretion.
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PMID:Cardiac secretion and renal clearance of atrial natriuretic peptide in normal man: effect of salt restriction. 253 79

Escape from the sodium-retaining effects of aldosterone (ALDO) is thought to occur as a result of natriuretic compensatory mechanisms triggered by extracellular fluid volume expansion. The purpose of the present study was to determine whether increases in plasma levels of atrial natriuretic peptide occur during ALDO escape in conscious dogs (n = 6) maintained on a fixed sodium intake (60 meq/day). Infusion of ALDO at a rate of 15 micrograms X kg-1 X day-1 for 6 days decreased sodium excretion (UNaV) from 59.1 +/- 4.0 to 36.2 +/- 5.7 meq/day on day 1, and then UNaV gradually returned to control levels by day 5 of ALDO infusion. Net cumulative sodium balance progressively increased during ALDO infusion, reaching a peak value of 88.8 +/- 21.3 meq/day on day 5. Mean arterial pressure increased from 85 +/- 3 to 95 +/- 4 mmHg, and plasma renin activity decreased from 1.32 +/- 0.27 to 0.32 +/- 0.07 ng angiotensin (ANG) I X ml-1 X h-1 during ALDO infusion. Plasma levels of atrial natriuretic peptide averaged 67.5 +/- 8.9 pg/ml during control and increased to a peak value of 120 +/- 18 pg/ml by day 4 of ALDO infusion. Three to four days after ALDO infusion was stopped, plasma levels of atrial natriuretic peptide averaged 46 +/- 5 and 50 +/- 6 pg/ml, respectively. In summary, escape from the sodium-retaining effects of ALDO is associated with significant increases in the circulatory levels of atrial natriuretic peptide.
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PMID:Elevated levels of atrial natriuretic peptide during aldosterone escape. 295 58

In previous studies it has not been possible to determine net intrarenal formation of angiotensin II (ANG II) from arteriovenous ANG II concentrations because of the high intrarenal ANG II degradation rates (DR). This study was designed to determine ANG II-DR and to estimate net intrarenal ANG II formation during normal and enhanced renin secretion rate (RSR). In anesthetized dogs, plasma renin activity and ANG II were measured in arterial and renal venous blood by radioimmunoassay during four periods: control, renal arterial constriction (RAC), angiotensin converting enzyme (ACE) inhibition (MK 422), and MK 422 plus systemic arterial ANG II infusion. ANG II-DR was determined in each dog from the arterial-renal venous ANG II concentration difference during the period of ANG II infusion in the presence of ACE inhibition; this value was used to estimate net ANG II formation by predicting the amount of arterially delivered ANG II that escaped degradation. The average percent ANG II-DR calculated during ANG II infusion (range of 0.05 to 0.20 microgram/min) was 89 +/- 2%. In response to RAC, RSR increased from 11 +/- 3 to 24 +/- 5 ng ANG I X h-1 X min-1 X g-1. Arterial ANG II (67 +/- 11 pg/ml) and renal venous ANG II (29 +/- 6 pg/ml) increased to 133 +/- 18 and 61 +/- 10 pg/ml, respectively. Net intrarenal ANG II formation increased from 44 +/- 11 to 83 +/- 13 pg X min-1 X g-1 after renal arterial constriction. There was a significant relationship between the change in RSR and the change in ANG II formation rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:De novo intrarenal formation of angiotensin II during control and enhanced renin secretion. 303 44

We administered the diuretics furosemide and ethacrynic acid to conscious freshwater turtles to assess changes in renal function and plasma renin activity (PRA) in an animal which lacks a loop of Henle. Furosemide (2 and 5 mg/kg) produced no changes in blood pressure, hematocrit, plasma electrolytes, glomerular filtration rate (GFR), or PRA. Furosemide doubled urine volume while sodium excretion increased 20-fold and chloride and potassium excretion increased 12-fold (P less than 0.05 in each case). Net potassium secretion was observed. Ethacrynic acid (2 and 5 mg/kg) also produced no changes in blood pressure, hematocrit, plasma electrolytes, or PRA. At the lower dose GFR increased by 40% and urine volume nearly doubled (P Less than 0.05 in each case). Sodium, chloride, and potassium excretion increased roughly 10-fold (P less than 0.05 in each case). At the higher dose, GFR increased by 80% and urine volume more than doubled (P Less than 0.05 in each case). Sodium excretion rose 40-fold, chloride excretion rose 25-fold, and potassium excretion rose 10-fold (P less than 0.05 in each case). At both doses net potassium secretion occurred. The results demonstrate that both drugs inhibit tubular reabsorption in the turtle, acting primarily on distal segments of the nephron. The failure of either drug to alter PRA suggests that the turtle lacks a tubular mechanism for altering renin release.
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PMID:Renal responses to diuretics in the turtle. 391 2

Urinary acidification was studied in six unrelated infants with fetal alcohol syndrome and eight healthy age-matched infants. Creatinine clearance, fractional sodium excretion, plasma renin activity, and plasma aldosterone were normal in all patients but fractional potassium excretion was lower in the patients than in the controls (p = 0.0001). After ammonium chloride loading, minimum urine pH was significantly higher in FAS patients than in control subjects (5.5 +/- 0.1 and 4.7 +/- 0.1, respectively, p = 0.00005). Net acid excretion was also lower in the patients (24.5 +/- 1.7 Eq/min) than in the controls (27.8 +/- 2.1 Eq/min, p = 0.008). Following sodium bicarbonate loading, fractional bicarbonate excretion was significantly higher (p = 0.00005) and fractional potassium excretion significantly lower (p = 0.002) in the patients than in the controls with comparable blood pH and bicarbonate levels. Treatment with chlorothiazide lowered plasma potassium and raised plasma bicarbonate to normal levels (p = 0.05). Concomitantly, fractional sodium excretion, fractional potassium excretion, and urinary net acid excretion increased significantly (p = 0.01). We conclude that patients with fetal alcohol syndrome have a defect in distal acidification and potassium excretion which cannot be attributed to abnormal aldosterone secretion.
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PMID:Impaired renal acidification in infants with fetal alcohol syndrome. 404 Oct 29

This study was performed to determine whether there is any difference in cation transport of red blood cells from normotensive subjects and hypertensive patients in Japan. Net Na+ efflux and net K+ influx rates were measured in sodium-loaded red cells from 19 normotensive subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na+/K+ net fluxes and the net cation flux rate were compared between these groups. The ratio of Na+/K+ net fluxes was significantly lower in essential hypertensive patients than in normotensive subjects. Parameters such as age, sex, blood pressure, plasma renin activity, and plasma aldosterone concentration were also examined in 2 groups of essential hypertensive patients, divided on the basis of their Na+/K+ net fluxes. However, there is no significant difference between the groups. These results suggest that the ratio of cation flux is related to hypertension independently of these parameters.
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PMID:Cation transport of red blood cells from hypertensive patients in Japan. 636 95


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