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

Since recent investigations have shown elevated urinary PGE2 and polyuria in hypokalemic animals which were reversed by PG synthesis inhibition with indomethacin, studies were undertaken to examine the effects of extracellular [K+] on renomedullary PG production in vitro. Slices of rabbit and human renal papilla were incubated in Krebs-Ringer HCO3- buffer, 95% O2-5% CO2, glucose 10 mM, HSA 4 gm/100 ml, for 30 min at 38 degrees C, with and without 1-14C-AA (10 micrometer). Measurments were made of total endogenous iPGE2 and iPGF2alpha production and radioactive AA leads to PGE2. In rabbit renal medulla values for iPGE2 (nmol/gm/30 min) were 252 +/- 20 at [K+] 0; 182 +/- 17 at [K+] 2.5 mEq/L; 163 +/- 18 at [K+] 5.5; and 129 +/- 17 [K+] 9.0 (p less than 0.005). iPGF2alpha was unaltered by changes in media potassium concentrations (6.8 +/- 0.9 nmol/gm/30 min at [K+] 0 and 6.2 +/- 0.8 at [K+] 9.0 MEq/L). In the human renal medulla iPGE2 was 9.5 +/- 1.6 nmol/gm/30 min at [K+] 0; 5.0 +/- 0.7 at [K+] 2.5 mEq/L; 5.3 +/- 0.3 at [K+] 5.5; and 4.6 +/- 1.0 at [K+] 9.0 (p less than 0.05). AA leads to PGE2 (nmol/gm/30 min) was 3.21 +/- 0.92 at [K+] 0; 2.47 +/- 0.57 at [K+] 2.5 mEq/L; 1.30 +/- 0.30 at [K+] 5.5; and 0.76 +/- 0.4 at [K+] 9.0 in rabbit medulla (P less than 0.005). It is postulated that direct stimulation of papillary PGE2 biosynthesis by low extracellular [K+] impairing the cAMP-generating response to vasopressin could represent the initial event in the pathogenesis of vasopressin-resistant polyuria.
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PMID:Renal biosynthesis of prostaglandin E2 and F2alpha: dependence on extracellular potassium. 71 2

Abstract Effect of atrial natriuretic peptide (ANP) on the vasopressin response to osmotic stimulation (Experiment I) as well as to hemorrhage (Experiment II) was investigated in anesthetized dogs. Moreover, cardiovascular function and renal water and electrolyte excretion were studied. In Experiment I, 2.5 M NaCI, containing 0.02 mug.kg (1) of ANP, was infused intravenously at a rate of 0.2 ml.kg(-1), min (1) after one bolus injection of 0.75 mug.kg (1) ANP (HSA group). In the control group, 2.5 M NaCI alone (HS group) was infused. The infusion was continued for 75 min. In Experiment II, 0.15 M NaCI, containing the identical dose of ANP to Experiment I (HA group), or 0.15 M NaCI alone (H group) was infused intravenously during bleeding at a rate of 1 ml.kg(-1).min (-1) for 40 min. In Experiment I, infused ANP suppressed the vasopressin response to a mild osmotic stimulation, but not to a strong osmotic stimulation and attenuated ANP release and a rise in arterial and central venous pressures in response to plasma volume expansion, without the enhanced natriuresis. In Experiment II, infused ANP neither impaired the vasopressin response to bleeding nor potentiated a fall in mean arterial pressure and central venous pressure. In conclusion, ANP at physiological and/or supraphysiological range may suppress the vasopressin response to a mild osmotic stimulation, but not to a strong osmotic stimulation and to hemorrhage. In addition, ANP given intravenously may attenuate ANP release and a rise in blood pressure without any natriuresis.
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PMID:Effect of atrial natriuretic Peptide on the vasopressin response to osmotic and hemorrhagic stimuli in dogs. 1921 36