Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibition of prostaglandins (PGs) synthesis induces responses on renal function that are age-dependent. Indomethacin in the adult rat potentiates the response to vasopressin whereas in the newborn rat blocks the response to dehydration. These differences suggest that the sensitivity of the renal tissue to PGs changes as the animal matures. This study was designed to analyze the characteristics of the receptors to PGE2 in the developing rat and to compare with that of the adult rat. Binding was performed in cortical and medullary slices incubated with tritiated PGE2. It was found that the renal uptake of the radioactive ligand had three components, the first is the synthesis of endogenous prostaglandins, the second is tubular secretion (only in cortex) and the third is binding to receptor sites. We found it necessary to eliminate the first two components (with indomethacin and p-amino-hippurate) to achieve an adequate measurement of the apparent affinity of the binding sites to PGE2. Under these conditions the cortex bound more PGE2 than the medulla (at all ages) and the highest affinity was observed in the neonatal cortex. Synthesis of prostaglandin E2 was higher in newborn than in adult rats. In vivo, indomethacin and acetaminophen blocked the response of the newborn rat to dehydration whereas in the weaning and adult rat the response was not changed by these inhibitors of the synthesis of prostaglandins. Our results suggest a major role of the prostaglandins in the regulation of the water balance in the neonate.
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PMID:Development of the receptors to prostaglandin E2 in the rat kidney and neonatal renal functions. 256 Sep 67

Intravenous (i.v.) infusion of the selective vasopressin (V2) agonist 1-desamino-8-D-arginine vasopressin (DDAVP, Desmopressin) in humans causes a fall in blood pressure, an increase in heart rate, and a rise in plasma renin and noradrenaline. The present study was designed to demonstrate the vasodilatory properties of DDAVP in the renal circulation and to describe the effect of DDAVP on renin secretion. Seven male subjects (31-63 years) with hypertension, who showed no signs of renal parenchymal disease, received an i.v. infusion of DDAVP (400 ng/kg in 10 minutes). They were studied at the time they were undergoing renal vein renin sampling and renal angiography as part of the diagnostic work-up of their hypertension. 131I-Hippurate clearance was used to measure effective renal plasma flow (ERPF). True renal plasma flow was calculated as ERPF divided by the renal extraction ratio of 131I-hippurate. 125I-Thalamate clearance was used to measure glomerular filtration rate (GFR). Measurements were made before and 15-20 minutes after administration of DDAVP. Angiography was performed in the same session after the last blood samples had been collected. In all patients the renal arteries were normal and the extraction ratios of 131I-hippurate and 125I-thalamate (Ehip, Ethal) were not different for the left and right kidney, and in all seven patients a diagnosis of essential hypertension was made. After DDAVP systolic blood pressure decreased by 14.4 mmHg (2.0-26.8) (mean, 95% confidence interval, p < 0.05). Diastolic blood pressure decreased by 12.1 mmHg (2.9-21.7, p < 0.01). Heart rate increased by 17.5 bpm (11.7-23.2, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of DDAVP on renal hemodynamics and renin secretion in subjects with essential hypertension. 795 85

Effects of urodilatin (5, 10, 20, and 40 ng. kg-1. min-1) infused over 2 h on separate study days were studied in eight normal subjects with use of a randomized, double-blind protocol. All doses decreased renal plasma flow (hippurate clearance, 13-37%) and increased fractional Li+ clearance (7-22%) and urinary Na+ excretion (by 30, 76, 136, and 99% at 5, 10, 20, and 40 ng. kg-1. min-1, respectively). Glomerular filtration rate did not increase significantly with any dose. The two lowest doses decreased cardiac output (7 and 16%) and stroke volume (10 and 20%) without changing mean arterial blood pressure and heart rate. The two highest doses elicited larger decreases in stroke volume (17 and 21%) but also decreased blood pressure (6 and 14%) and increased heart rate (15 and 38%), such that cardiac output remained unchanged. Hematocrit and plasma protein concentration increased with the three highest doses. The renin-angiotensin-aldosterone system was inhibited by the three lowest doses but activated by the hypotensive dose of 40 ng. kg-1. min-1. Plasma vasopressin increased by factors of up to 5 during infusion of the three highest doses. Atrial natriuretic peptide immunoreactivity (including urodilatin) and plasma cGMP increased dose dependently. The urinary excretion rate of albumin was elevated up to 15-fold (37 +/- 17 micrograms/min). Use of a newly developed assay revealed that baseline urinary urodilatin excretion rate was low (<10 pg/min) and that fractional excretion of urodilatin remained below 0.1%. The results indicate that even moderately natriuretic doses of urodilatin exert protracted effects on systemic hemodynamic, endocrine, and renal functions, including decreases in cardiac output and renal blood flow, without changes in arterial pressure or glomerular filtration rate, and that filtered urodilatin is almost completely removed by the renal tubules.
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PMID:Cardiovascular, endocrine, and renal effects of urodilatin in normal humans. 1007 Jan 28