AJP - Heart and Circulatory Physiology, Vol 250, Issue 4 584-H594, Copyright © 1986 by American Physiological Society
Cardiovascular and renal responses to chronic vasopressin infusion
A. J. Brown, T. E. Lohmeier, R. G. Carroll and E. F. Meydrech
Arginine vasopressin (AVP) was infused into the renal artery of seven
uninephrectomized conscious dogs at successive rates of 0.09, 0.36, and
1.46 ng X kg-1 X min-1 for 18, 9, and 5 days, respectively; subsequently,
the nonpressor analogue of AVP, 1-desamino-8-D-arginine vasopressin
(DDAVP), was infused intrarenally for 7 additional days. The lowest
infusion rate of AVP produced a high concentration of AVP in the renal
circulation (maximal antidiuresis) with only a relatively moderate increase
in peripheral plasma AVP concentration. For comparison, the effects of a
comparable increase in peripheral plasma AVP concentration during
intravenous infusion at this same rate were observed in an additional group
of dogs. Acutely, when this low dose of AVP was infused either intrarenally
or intravenously, there was marked antidiuresis, but there were no
significant changes in mean arterial pressure (MAP), renal hemodynamics, or
urinary electrolyte excretion. Chronically, in both groups of animals,
cumulative water balance was positive, and glomerular filtration rate,
effective renal plasma flow, and MAP (16-18 mmHg) all increased; plasma
renin activity decreased. Similar changes were observed during DDAVP
infusion. When elevated peripheral plasma levels of AVP were achieved
during the higher infusion rates of AVP, natriuresis and diuresis occurred,
but, otherwise there was little change in the above variables, including
MAP. Thus the hydrosmotic effects of AVP appear to account for its moderate
hypertensive activity. Further, the failure of AVP to produce prominent
hypertension, even when pronounced systemic vasoconstrictor effects are
manifested, may be a result of its inability to promote significant renal
vasoconstriction and antinatriuresis.
