Aw. Cowley et al., CHRONIC INTRAVENOUS ADMINISTRATION OF V-1 ARGININE-VASOPRESSIN AGONIST RESULTS IN SUSTAINED HYPERTENSION, The American journal of physiology, 267(2), 1994, pp. 80000751-80000756
Despite the well-recognized vasoconstrictor and fluid-retaining action
s of vasopressin, prolonged administration of arginine vasopressin (AV
P) to normal animals or humans fails to produce sustained hypertension
. The present study was performed to elucidate the role of the V-1 rec
eptor in determining the ability of AVP to produce sustained hypertens
ion. Conscious Sprague-Dawley rats with implanted catheters were infus
ed with the selective V-1 agonist, [Phe(2),Ile(3), Orn(8)]vasopressin
(2 ng.kg(-1).min(-1)), for 14 days in amounts that were acutely nonpre
ssor. Blood pressure (MAP), heart rate (HR), body weight, and water in
take (WI) were determined daily. Plasma AVP, plasma catecholamines nor
epinephrine and epinephrine, plasma osmolality, and electrolyte concen
tration were determined before and on days 1 and 7 of infusion. MAP in
creased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/-
5 mmHg above control by day 14 (transient decrease on days 6-9) and t
hen fell to control levels after the infusion was stopped. HR did not
change significantly. Plasma AVP immunoreactivity increased from 2.5 /- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall on
ly on clay 1, with epinephrine only slightly elevated on day 7. No evi
dence of fluid retention was found, and rats lost sodium only on the f
irst day of V-1 agonist infusion. Body weight increased throughout the
study but was unrelated to the changes of MAP. We conclude that chron
ic stimulation of V-1 receptors results in sustained hypertension in r
ats.