AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 5 1217-R1225, Copyright © 1994 by American Physiological Society
Prolonged stimulation of intrarenal V1 vasopressin receptors results in sustained hypertension
E. Szczepanska-Sadowska, K. Stepniakowski, M. M. Skelton and A. W. Cowley Jr
Medical Academy of Warsaw, Poland.
In an earlier study, we reported that chronic intravenous administration of
the V1 agonist [Phe2,Ile3,Orn8]vasopressin (V1AG) results in sustained
hypertension. The present study was designed to determine whether
V1-induced hypertension may be related specifically to intrarenal actions
of this peptide. Chronic infusion of the V1 agonist into the medullary
interstitial space of a single remaining kidney of normal, conscious
Sprague-Dawley rats at the rate of 2 ng.kg-1.min-1 for 14 days resulted in
a sustained rise of 18 mmHg of mean arterial pressure (MAP). After
withdrawal of V1AG, MAP returned to the baseline level. During the first
day of V1AG infusion, there was a net loss of body sodium and no evidence
of fluid retention throughout the period of hypertension. Plasma
osmolality, sodium and potassium concentration, and water intake and body
weight were not significantly affected by medullary interstitial infusion
of V1AG. Renal medullary interstitial infusion of an equimolar amount of
arginine vasopressin (AVP) did not affect MAP. Chronic medullary
interstitial infusion of the selective V1 antagonist
d(CH2)5[Tyr(Me)2,Ala-NH(2)9]AVP in equimolar amounts (2.5 ng.kg-1.min-1)
prevented the MAP increase elicited by intravenous V1AG. However,
intravenous administration of the V1 antagonist at the same rate together
with V1AG (n = 7) failed to prevent hypertension. The results indicate that
hypertension can be elicited by chronic stimulation of renal medullary V1
vasopressin receptors. They also suggest that some V2 agonistic properties
of AVP may restrict the hypertensive action of this hormone. The mechanism
for the rise of arterial pressure remains to be determined.
