EFFECTS OF V-1-VASOPRESSIN AND V-2-VASOPRESSIN (AVP) ANTAGONISTS ON THE PRESSOR, AVP AND ATRIAL-NATRIURETIC-PEPTIDE RESPONSES TO A HYPERTONIC SALINE INFUSION IN CONSCIOUS ANEPHRIC RATS

Citation
K. Ota et al., EFFECTS OF V-1-VASOPRESSIN AND V-2-VASOPRESSIN (AVP) ANTAGONISTS ON THE PRESSOR, AVP AND ATRIAL-NATRIURETIC-PEPTIDE RESPONSES TO A HYPERTONIC SALINE INFUSION IN CONSCIOUS ANEPHRIC RATS, European journal of endocrinology, 133(1), 1995, pp. 127-132
Citations number
26
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
08044643
Volume
133
Issue
1
Year of publication
1995
Pages
127 - 132
Database
ISI
SICI code
0804-4643(1995)133:1<127:EOVAV(>2.0.ZU;2-W
Abstract
To examine the role of vasopressin (AVP) receptors in the regulation o f the hemodynamics and release of atrial natriuretic peptide (ANP), an d the participation of renal nerve inputs in the osmotic AVP release, hypertonic saline (HS) was infused into conscious, bilaterally nephrec tomized rats with nonpeptide, selective antagonists for the V-1-recept or or V-2-receptor of AVP. In the control group, HS alone increased me an arterial pressure, plasma ANP and AVP, plasma volume and plasma osm olality, and decreased the heart rate. In the V-1-receptor antagonist group, an increase in the mean arterial pressure and a decrease in hea rt rate were completely abolished and an increase in plasma ANP was at tenuated. In the V-1-receptor antagonist group, increases in mean arte rial pressure and plasma ANP and a decrease in heart rate were attenua ted. However, the ratio of the changes in heart rate to the changes in mean arterial pressure in the V-2-receptor antagonist group is signif icantly higher than that in the control group. In both experimental gr oups, increases in plasma AVP, plasma volume and plasma osmolality wer e not different from those in the control group. These results suggest that a HS-induced increase in mean arterial pressure is mediated by t he presser effect of AVP, mainly through V-1-receptors, and that the d epressor effect of AVP through V-2-receptors may not influence tonical ly HS-induced hypertension, Moreover, HS-induced increase in plasma AN P is mediated mainly by increases in plasma volume and blood pressure, but may not be affected by a direct action of AVP to the heart. Renal afferent nerve inputs may not have effects on the regulation of osmot ic AVP release.