PMID: 11330329May 2, 2001Paper

High concentrations of oxytocin cause vasoconstriction by activating vasopressin V1A receptors in the isolated perfused rat kidney

Naunyn-Schmiedeberg's Archives of Pharmacology
C LoichotM Barthelmebs

Abstract

The aim of this study was to evaluate the renal vascular effects of oxytocin in Sprague-Dawley rats and in Brattleboro heterozygous or homozygous rats, the latter being genetically deficient in vasopressin synthesis. Studies were performed in vitro, in the isolated kidney perfused in an open circuit with a Tyrode's solution. Oxytocin induced a concentration-dependent renal vasoconstriction in Sprague-Dawley rats, at rather high concentrations (EC50=170+/-39 nM, mean +/- SEM, n=6) with a maximum response amounting to 44% of that elicited by vasopressin (increase in renal vascular resistance: 11.5+/-0.9 mmHg min ml(-1) vs. 26.2+/-2.2 mmHg min ml(-1)). Oxytocin-evoked renal vasoconstriction was abolished by SR 49059, a selective vasopressin V1A receptor antagonist (10 nM), but not by d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr-(NH2)9] vasotocin, an oxytocin receptor antagonist (10 nM). In the presence of SR 49059, oxytocin did not induce renal vasorelaxation. Oxytocin induced renal vasoconstriction in Brattleboro homozygotes and heterozygotes (EC50=59+/-12 nM and 262+/-110 nM; Emax=7.8+/-1.1 mmHg min ml(-1) and 6.9+/-0.4 mmHg min ml(-1), n=5 respectively) with characteristics similar as observed in Sprague-Dawley rats concerning partial agonis...Continue Reading

Citations

Nov 5, 2010·PloS One·Bogdan A DanalacheMarek Jankowski
Aug 21, 2012·Experimental Physiology·Michael Brian SantiagoAlexandre Giusti-Paiva
Oct 30, 2016·Peptides·Mirali PolshekanYaghoub Yazdani
Oct 25, 2016·Physiological Research·A Puzserova, I Bernatova
Sep 24, 2019·Current Neuropharmacology·Nina Japundžić-ŽigonDavid Murphy

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