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 effect of reduced blood flow in the liver was studied in acute and chronic experiments on rats. 2 hours after partial constriction of the portal vein in anesthetized rats the mean blood pressure was lower and the plasma renin activity higher than in the control group. There was no relation between the two parameters. 20 weeks after partial constriction of the portal vein in unanesthetized animals the body weight, liver weight and serum albumin fraction were decreased, while the kidney weight was increased significantly and the heart weight insignificantly. The systolic blood pressure of these animals was found to be lower than that of the controls, and their blood pressure response to the i. v. administration of angiotensin II was also lower. In comparison with the control no significant differences were found in the blood renin and substrate levels. The natriuresis proved considerably lower in the animals with the partial constriction of the portal vein.
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PMID:[Effect of decreased blood flow in the liver on blood pressure and on the renin-angiotensin system of the rat]. 668 68

Six patients with alcoholic liver disease and massive ascites were treated by dialytic ultrafiltration and peritoneal reinfusion of their ascitic fluid. Immediately after the procedure there was significant improvement in cardiac output (5.2 +/- 0.4 to 5.9 +/- 0.4 L/m, p less than 0.05) and stroke volume (53 +/- 5.5 to 62 +/- 4.7 ml/beat, p less than 0.02) with no change in heart rate or blood pressure, right atrial, pulmonary artery, or wedge pressures. Serum creatinine and serum electrolytes were stable. Ascitic fluid albumin rose significantly immediately after the procedure (1.5 +/- 0.2 to 2.9 +/- 0.5 g/dl, p less than 0.001) with gradual improvement in serum albumin (2.9 +/- 0.3 to 4.1 +/- 0.2 g/dl, p less than 0.05) in 3 months. Plasma renin (26.9 +/- 9.6 to 17.9 +/- 6.3 ng/ml/h, p less than 0.05) and plasma aldosterone (67 +/- 18 to 39 +/- 11 ng/dl, p less than 0.01) fell significantly immediately after the procedure. No serious side effects were noted and liver function remained stable. Four of six patients followed for 3-14 months could be managed on lower doses of diuretics.
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PMID:The effects of dialytic ultrafiltration and peritoneal reinfusion in the management of diuretic resistant ascites. 671 32

This study examined body fluid volumes, the pressor responses to norepinephrine (NE), and the cardiovascular responses to NE before and during infusion of an angiotensin II (ANG II) antagonist in two-kidney rabbits with unilateral renal artery stenosis (RAS) of 3 and 30 day duration. Three separate experiments were performed. In the first experiment, plasma volume, extracellular fluid volume, and total body water were measured by the distribution volumes of radioiodinated serum albumin, 35SO4, and tritiated water, respectively. No differences were seen for any of these volumes between the 3- or 30-day RAS rabbits and their controls. In the second experiment, pressor responses to infusions of several doses of NE were examined; rabbits with 3- and 30-day RAS had exaggerated pressor responses to all doses of NE when compared with the control rabbits. In the third experiment, infusion of NE at 800 ng.min-1.kg body wt-1 resulted in more pronounced increases in mean arterial pressure and total peripheral resistance (TPR) in the 3- and 30-day RAS rabbits than in the controls; after infusion of [Sar1-Ile8] ANG II the increases in mean arterial pressure and TPR during NE infusion were blunted and were of the same magnitude as in the control group. In all experiments the 30-day RAS rabbits were hypertensive, whereas the 3-day RAS rabbits were normotensive; also, plasma renin activity (PRA) values were normal in both the 3- and 30-day RAS groups. These studies demonstrated that increases in body fluid volumes are not necessary for pressor and vascular hyperresponsiveness probably is mediated by ANG II, despite normal PRA values.
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PMID:Fluid volumes and pressor responsiveness in two-kidney rabbits with renal artery stenosis. 675 10

The effect of water deprivation on the osmotic release of renin was evaluated in conscious rats previously prepared with right nephrectomy and cannulations of left renal artery and lower abdominal aorta. The osmotic signal was a 4-min intrarenal infusion of 30% crystallized bovine serum albumin. Changes in aortic plasma concentration of renin (PRC) and total protein were followed serially. In normal hydropenic rats an increase in PRC was not detected with the oncotic challenge. Following a 48-hr period of water deprivation, the same external oncotic signal increased PRC threefold above baseline within 3 min. It is concluded that some intrarenal functional or structural change induced by water deprivation sensitizes the renin-secreting mechanism to colloid osmotic stimuli. It is suggested that this change could be related to the physical conditions of the renal interstitium.
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PMID:The effect of water deprivation on the osmotic release of renin. 675 28

Body fluid volumes and their relation to mean arterial pressure and plasma renin activity (PRA) were examined in heminephrectomized rats after 4 wk of treatment with deoxy-corticosterone acetate (DOCA) and placed on one of three levels of salt intake, either high (D-HS), normal (D-NS), or low (D-LS); sham-operated rats, which received heminephrectomy and no DOCA treatment, also received high (S-HS), normal (S-NS), or low (S-LS) intakes of salt. Body fluid volumes were measured as the distribution volumes of radioiodinated serum albumin, 35SO4, and tritiated water for plasma volume (PV), extracellular fluid volume (EFV), and total body water (TBW), respectively. Approximately the same degrees of hypertension occurred in the D-HS and D-NS rats, but the D-LS rats were normotensive. PV and EFV were increased only in the D-HS rats, with no prominent changes occurring in the D-NS rats. Intracellular fluid volume (ICF) was not changed in the D-NS rats when compared with the S-NS rats. The ratios of PV/EFV and EFV/TBW in the DOCA-treated groups on high or normal salt were not different from their controls. PRA was greatly suppressed in the D-HS and D-NS rats when compared with all other groups. In another group of D-HS rats, sodium was restricted for 2 wk; in this group the mean arterial pressure fell to control levels without significant changes in PV, but interstitial fluid volume was reduced to normal levels. These results demonstrated that 1) in DOCA-salt hypertensive rats there is expansion of body fluid volumes that are proportionally distributed among the PV, EFV, and ICF; 2) increases in body fluid volumes are not necessary for DOCA to maintain hypertension; 3) a certain minimal amount of dietary sodium is necessary for the development and maintenance of hypertension; and 4) following DOCA treatment the suppression of PRA is not due solely to expansion of body fluid volumes.
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PMID:Body fluid distribution in the maintenance of DOCA-salt hypertension in rats. 684 57

Free aldosterone, the aldosterone precursor 18-OH-corticosterone, and 18-OH-deoxycorticosterone as well as the aldosterone metabolites 18-glucuronide and tetrahydroaldosterone were measured by radioimmunoassay in the urine of 24 children with the nephrotic syndrome. In addition renin activity, aldosterone and corticosterone were measured in plasma. All children with manifest edema showed increased values of one or more of the measured aldosterone parameters indicating hyperaldosteronism. In non-edematous patients one or more parameters were increased in 9 of 16 patients. Free aldosterone, tetrahydroaldosterone and 18-OH-corticosterone proved to be the most sensitive urinary parameters for the detection of increased mineralocorticoid function. Free urinary aldosterone was correlated with sodium excretion and with serum albumin. The pathogenesis of hyperaldosteronism in the nephrotic syndrome and its role in the development of edema are discussed.
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PMID:Mineralocorticoids in the nephrotic syndrome of children. 701 53

Hypertensin occurred 24 to 48 hours after resuscitation in 35 of 86 injured patients, who had combined systolic and diastolic hypertensin (150/100 mmHg) for six or more consecutive hours. Plasma volume (PV), RBC volume, extracellular fluid (ECF) volume by the inulin dilution technique, renal plasma flow, glomerular filtration rate, and peripheral renin levels were measured in hypertensive and nonhypertensive patients an average of 40 hours after injury. The hypertensive patients had an average mean arterial pressure (MAP) of 114 mmHg, compared with 95 mmHg in the nonhypertensive patients. The RBC volume and ECF were comparable for both groups, whereas PV was increased in the hypertensive patients (3.6 L vs 3.3 L). Calculated interstitial fluid space (IFS) volume was greater in the nonhypertensive patients, as was the ratio PV/IFS. The MAP in both groups correlated directly with PV/IFS and serum albumin concentrations, and inversely with peripheral renin concentrations. This suggests that postresuscitative hypertension is not due to fluid overload but rather to the fluid maldistribution related to altered IFS compliance as reflected by the increased PV/IFS.
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PMID:Altered interstitial fluid space dynamics and postresuscitation hypertension. 701 68

Renin release was measured in the isolated rat kidney perfused with a recirculating artificial medium containing bovine serum albumin at 6.7 g per 100 ml of 11 g per 100 ml. At the higher concentration of albumin, glomerular filtration ceased and the rate of renin release over 70 minutes of perfusion was increased 6-fold. The addition of ouabain to the perfusate containing 11 g per 100 ml inhibited the release of renin, suggesting that inhibition of Na-K-ATPase or the related changes in cellular volume or composition prevented renin release. Lowering the osmolality of the perfusate by reducing the concentration of sodium chloride also prevented the increase in renin secretion produced by perfusion with 11 g per 100 ml albumin. Increasing the osmolality of the perfusate with mannitol restored the augmented renin release. These results are consistent with the hypothesis that alterations in the volume of certain cells, perhaps in the juxtaglomerular apparatus itself, can control renin release.
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PMID:Stimulation of renin release by hyperoncotic perfusion of the isolated rat kidney. 703 19

Twenty-three patients with premature uterine contractions occurring between the 27th and 35th weeks of pregnancy were treated in a prospective and randomized study with intravenous ritodrine in a 0.1 wt/vol% solution of isotonic saline (N = 12) or isotonic glucose (N = 11). The aim of the study was to record the effects of these agents on the water-salt metabolism. In both the saline and the glucose groups there was a statistically significant fall in hemoglobin, hematocrit, and serum albumin (P less than .001). This fall correlated significantly with the dose of ritodrine (P less than .001). Serum renin and aldosterone levels revealed a statistically significant increase (P less than .0005). Seven of 12 patients in the saline group, but none in the glucose group, developed pulmonary congestion requiring treatment. The combination of ritodrine and saline should be used very cautiously, and the authors recommend accurate monitoring of the fluid balance during ritodrine treatment.
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PMID:Pulmonary edema following ritodrine-saline infusion in premature labor. 726 50

To determine the clinical significance of plasma endothelin-1 in chronic liver disease, these levels were measured by radioimmunoassay. The plasma endothelin-1 levels in patients with cirrhosis (N = 16) (2.04 +/- 0.25 pg/ml) and patients with hepatocellular carcinoma (N = 22) (2.23 +/- 0.17 pg/ml) increased significantly compared with controls (N = 16) (1.17 +/- 0.17 pg/ml) and patients with chronic hepatitis (N = 11) (1.09 +/- 0.19 pg/ml) (P < 0.01). The presence of ascites rather than tumor volume was associated with a significant elevation of endothelin-1. Endothelin-1 showed significant negative correlations with parameters of hepatic function, including indocyanine green clearance, serum albumin, and prothrombin time. Although endothelin-1 was not correlated with plasma renin activity and plasma endotoxin, it demonstrated a significant positive correlation with the plasma level of atrial natriuretic peptide (r = 0.42, P < 0.01). These findings demonstrate that plasma endothelin-1 increased in proportion to the severity of liver damage and may be causally related with the derangement of systemic/renal hemodynamics and fluid and electrolyte homeostasis seen in advanced liver disease.
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PMID:Clinical significance of plasma endothelin-1 in patients with chronic liver disease. 799 94


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