The
antidiuretic hormone,
arginine-vasopressin (AVP), may participate in the regulation of blood pressure (BP) through its
vasoconstrictor effects. In anesthetized rats, exogenous AVP induced stronger vasoconstriction in the mesenteric than in the renal vascular bed. Conversely, mesenteric but not renal vascular resistance was reduced by a vascular antagonist of AVP, d(CH2)5
VDAVP, in rats with increased endogenous AVP after
anesthesia,
dehydration, or injection of
glycerol. Another vascular AVP-antagonist, d(CH2)5
Tyr (Me) AVP, induced a transient fall in BP in conscious primates (marmosets) after
diuretic-induced volume depletion. In conscious rats with established
deoxycorticosterone acetate (
DOCA)/
salt hypertension, d(CH2)5
Tyr (Me) AVP decreased systolic BP after acute administration. After chronic administration of this antagonist during 6 weeks after the beginning of
DOCA/
salt treatment, the severity of
hypertension was reduced. When another, AVP-antagonist, d(CH2)5-D-Tyr (Et) VAVP, which blocks vascular and renal tubular AVP-receptors, was administered chronically, the development of
DOCA/
salt hypertension was prevented at the expense of severe and persistent
hypernatremia. These results demonstrate that under certain conditions the vascular effects of AVP may contribute to the maintenance of BP, AVP appears to participate in the pathogenesis of
DOCA/
salt hypertension through both its
vasoconstrictor and its
antidiuretic effects.