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 undertaken to explore the effects of chronic low-level cadmium ingestion in Dahl hypertension-resistant (R) and hypertension-sensitive (S) lines of rats. Groups of weanling female R and S rats were given 0 or 1 mg cadmium/1. in drinking water and fed either a low salt (0.4% NaCl) or a high salt (4% NaCl) diet for 28 weeks. Cadmium produced hypertension associated with gross cardiac hypertrophy and mild to moderate renal vascular changes in S, but not in R, rats on a low salt diet. Cadmium enhanced the rate and degree of development of salt-induced hypertension without exacerbating the hypercholesterolemia or renal vascular lesions normally observed in S rats on a high salt diet. Cadmium lowered circulating cholesterol levels in both lines on a low salt diet. Cadmium had no influence on growth, blood urea nitrogen concentration, plasma renin activity, tumor formation, or survivorship in R and S rats on either salt diet. This study indicates that the genetic composition is a critical determinant of the adverse effects of chronic low-level cadmium ingestion in rats. In addition to the experimental implications, these findings may have relevance to the problem of human "essential" hypertension.
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PMID:Effects of cadmium ingestion in rats with opposite genetic predisposition to hypertension. 48 40

Techniques are described in detail for the radioimmunological measurement of prostaglandin (PG) E2 and F2alpha in human urine. 50 ml urine samples are extracted with an organic solvent system and then purified by silicic acid column chromatography. The overall recovery after extraction and purification, calculated with labeled as well as unlabeled compounds, is in the order of 70%. The column eluates are assayed at 1:12-1:60 dilution in the "standard diluent" of the assay: 8 pg PGE2 or PGF2 alpha/ml of whole urine represents the lowest measurable concentration. A urine blank and a solvent blank were evaluated separately, subjecting 50 ml of urine obtained from an indomethacin treated subject ("PG-free" urine) or 50 ml of distilled water, respectively, to the extraction-purification procedures. Both were found not to interfere with the antigen-antibody reaction. Urinary PG-like immunoreactivity (LI) was characterized in terms of immunochemical and thin-layer chromatographic (TLC) behavior. Both urinary PGE2-LI and PGF2 alpha-LI behaved as authentic PGE2 and PGF2 alpha, upon dilution and on TLC. In 33 healthy female subjects (aged 19-58 yr), urinary excretion rates averaged 178 +/- 80 (mean +/- SD) ng/day for PGE2 and 498 +/- 181 ng/day for PGF2 alpha. In a group of 8 healthy men, both PGE2 and PGF2 alpha excretion rates were higher and more scattered than the female values. When two healthy women were given indomethacin (200 mg/day), urinary PGE2 and PGF2 alpha dropped to undetectable levels during the 4th day of drug therapy. Intravenous injection of furosemide (50 mg) in a female volunteer was followed by an immediate rise of urinary sodium, PGE2, PGF2 alpha and PGE2/PGF2 alpha ratio and plasma renin activity. In a 10 year old girl with Bartter's syndrome, urinary PG excretion rate was elevated with a 3 times higher than normal PGE2/PGF2 alpha ratio. Indomethacin therapy resulted in a prompt drop of PG excretion rate and of plasma renin activity. These results show that a combination of adequate purification steps and antisera with optimal characteristics provides a reliable method for measuring PGE2 and PGF2 alpha in urine, and therefore a valuable tool to further our knowledge of the physiology and physiopathology of the renal PG-system.
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PMID:Radioimmunoassay measurement of prostaglandins E2 and F2alpha in human urine. 48 26

To estimate the contribution of the specific defect in proximal and distal tubular reabsorption of sodium to renal salt wasting, fractional sodium excretion, distal tubular sodium delivery, and distal tubular sodium reabsorption were determined in 11 healthy premature infants. The study was performed on the seventh day and at weekly intervals thereafter up to the sixth week of life. Sodium clearance and fractional sodium excretion decreased significantly with increasing postnatal age (P less than 0.001). There was no significant alteration in either osmolar or free-water clearances. Distal tubular sodium delivery steadily decreased from 4.96 +/- 0.66 (mean +/- SE) in the first week to 3.3 +/- 0.41 ml/minute/dl GFR in the sixth week of life (P less than 0.05). Distal tubular sodium reabsorption was 69.5 +/- 2.36% in the first week, then rose significantly to reach a value of 83.7 +/- 1.85% in the second week (P less than 0.001) and remained practically unchanged thereafter. It is suggested that the rapid improvement of distal tubular sodium reabsorption in premature infants might result from forced stimulation by the excessively activated renin-angiotensin-aldosterone system.
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PMID:Postnatal development of renal sodium handling in premature infants. 49 Feb 50

1. Dietary sodium depletion and subsequent repletion was studied in rabbits. Potassium intake was maintained constant. 2. during sodium depletion and repletion blood pressure, packed cell volume, food consumption and body weight remained at control values. 3. Decreased sodium excretion was observed in both urine and faeces during sodium depletion and the physiological control of these changes is discussed in relation to the renin-angiotensin-aldosterone system. 4. Potassium excretion during sodium depletion initially fell as a result of reduced urine volume and gradually returned to normal. Urine potassium concentration remained constant. 5. Faecal excretion of potassium rose by 63% during sodium depletion and there was a rise from a control value of 17-25% in the proportion of total potassium excretion accounted for by the faecal component. 6. Water consumption and urine volume both decreased in the initial phase of sodium depletion and then returned to control levels. 7. It is important to consider both urinary and faecal excretion of sodium and potassium when calculating balance status for either ion. Faecal excretion, as well as kidney function, shows important physiological adaptations.
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PMID:Sodium, potassium and water metabolism in the rabbit: the effect of sodium depletion and repletion. 49 Mar 71

1. Active and acid-activatable (inactive) renins were measured in rabbit plasma under control conditions and during sodium depletion with subsequent repletion. 2. Active renin increased by 97% during sodium depletion and returned to control levels on repletion. Both changes were complete within 1 day of changing the diet. 3. During dietary sodium depletion inactive renin levels initially fell to zero and then increased until, after 13 days, inactive renin was again 10% of total renin levels, a proportion comparable to the control values. 4. Sodium repletion caused plasma inactive renin to return to control levels over about 13 days, a quite different time course to active renin. Therefore, in the first phase of repletion the proportion of total renin in the inactive form rose to 19%. 5. These changes are discussed in relation to concurrent changes in sodium, potassium and water metabolism.
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PMID:Plasma active and inactive renin in the rabbit: effect of dietary sodium depletion and repletion. 49 Mar 74

Plasma renin activities (resting PRA, post-dialysis delta PRA) were studied in 61 patients under chronic dialysis treatment. Removed sodium and removed water were estimated at each dialysis. Delta PRA/removed-sodium and delta PRA/removed-water were calculated as indices in response to the removal of sodium and water during the dialysis. 1)Resting PRA (pre-dialysis PRA) was positively correlated to delta PRA/removed-sodium, delta PRA/removed-water, serum osmolality, and diastolic blood pressure, but negatively to serum sodium concentration, age, and pulse pressure/diastolic blood pressure. Statistically significant factors controlling the resting PRA were delta PRA/removed-sodium, delta PRA//removed-water, and serum sodium concentration. Resting PRA was slightly correlated to diastolic blood pressure and age. 2)Post-dialysis PRA was significantly correlated to the resting PRA, delta PRA/removed-sodium, delta PRA/removed-water, serum sodium concentration, and age, but not to the blood pressure indices.
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PMID:Factors influencing the release of renin in patients under chronic dialysis treatment. 49 68

The importance of salt and water in the pathophysiology of the hypertensive state is well recognized. The current study is the first to report simultaneous measurements of red blood cell mass, plasma volume, extracellular fluid and total body water levels. Studies were performed in 82 white men, 14 with normal blood pressure and 16 with low renin and 52 with normal renin hypertension. The results indicate that subjects with normal renin hypertension compared with age-matched controls are characterized by an absolute increase (1.5 liter/m2) in intracellular fluid (total body water minus extracellular fluid). Furthermore, the ratio of extracellular fluid to total body water is decreased (0.43 to 0.38). No volume differences were found between subjects with low renin hypertension and age-matched subjects with normal renin hypertension. We conclude that subjects with normal renin hypertension compared with age-matched peers are characterized by an expanded intracellular fluid and that subjects with low renin hypertension do not exhibit a unique volume disorder.
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PMID:Volume studies in men with mild to moderate hypertension. 49 11

The effects of continuous intrarenal prostaglandin E2 (PGE2) infusion (7 days) on sodium and water balance, plasma renin activity (PRA), and sodium and water balance, plasma renin activity (PRA), and mean arterial pressure (MAP) were examined in conscious, unilaterally nephrectomized dogs maintained on a fixed sodium intake of 55 meq/day. PGE2 infusion (2 microgram/min) resulted in a sustained threefold increase in both urine output and water intake without a measurable change in glomerular filtration rate. PRA increased from 0.4 +/- 0.1 during the control period to 2.2 +/- 0.9 ng AI.ml-1.h-1 on day 1 and averaged 3.6 +/- 0.5 for the remaining 6 days of PGE2 infusion. Concurrently, MAP increased from 102 +/- 3 to a maximum of 117 +/- 4 mmHg on day 5; changes in PRA and MAP were significantly correlated (r = 0.96, P less than 0.001). Sodium excretion increased from 54.5 +/- 3 to 88.0 +/- 19 meq/day on day 1, and then declined to an average of 64.8 +/- 1 meq/day for the remaining 6 days of infusion. All variables returned to the control level during the recovery period. Intravenous infusion of PGE2 (2 microgram/min) yielded directionally similar but statistically insignificant effects. It is concluded that chronic intrarenal PGE2 infusion results in marked diuresis, polydipsia, a moderate loss of sodium, enhanced PRA, and mild hypertension.
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PMID:Prostaglandin E2-induced hypertension in conscious dogs. 49 30

After the administration of 40 mg Bay g 2821, a new potent diuretic substance, a significant increase of sodium and water diuresis occurred. There was only a short rise in potassium excretion. In contrast to the sodium and water diuresis no significant increase of renin-activity, angiotensin-II or aldosterone concentration was seen. In spite of the insignificant stimulation of the renin-angiotensin-aldosterone system, a significant increase of correlation occurred between the three components of the renin-angiotensin-aldosterone system.
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PMID:Changes of electrolyte excretion, renin activity, angiotensin-II and aldosterone concentrations during administration of 3-amino-1-(3,4-dichloro-a-methyl-benzyl)-2-pyrazolin-5-one (Bay g 2821). 51 20

1. The effect of restricted water intake followed by voluntary rehydration with water or 10 mM-KCl was studied in four conscious sheep with respect to plasma concentrations of renin, antidiuretic hormone (ADH), protein and electrolytes, and urine flow rate, osmolality and osmolal excretion. 2. Water restriction increased the plasma renin concentration and the plasma ADH concentration. 3. Rehydration with water caused a further rise in plasma renin, but plasma ADH returned to basal levels in less than 2 hr. 4. Rehydration with 10 mM-KCl in order to stabilize plasma K concentration greatly attenuated the post-drinking rise in plasma renin concentration, while plasma ADH levels fell as before. 5. Urine flow rates after rehydration with water and 10 mM-KCl remained low for at least 6 hr in most experiments despite low plasma ADH levels. The effect on urine osmolality ranged from no change to a large drop. 6. The post-drinking antidiuresis was associated with a reduction in solute excretion rate. However, free water clearance usually remained negative. 7. These experiments do not support the existence of a direct nexus between plasma ADH levels and plasma renin concentration.
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PMID:Renin, antidiuretic hormone and the kidney in water restriction and rehydration. 51 41


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