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
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
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.