AJP - Heart and Circulatory Physiology, Vol 258, Issue 3 722-H728, Copyright © 1990 by American Physiological Society
Arginine vasopressin increases apparent whole body capacity in anesthetized cats
D. S. Martin and J. R. McNeill
Department of Pharmacology, University of Saskatchewan, Saskatoon, Canada.
The effects of arginine vasopressin (AVP) on capacitance function were
assessed in anesthetized cats by draining blood from the superior and
inferior venae cavae into an external reservoir and then returning blood to
the right atrium at a constant rate. Under these conditions, changes in
reservoir volume were assumed to reflect reciprocal changes in whole body
capacity. Intravenous infusions of AVP (1, 10, and 100 ng.kg-1.min-1) that
elevated plasma AVP concentrations by approximately 30, 400, and 4,000
fmol/ml were associated with concentration-dependent increases in whole
body capacity that ranged between 1.6 and 8 ml/kg. In contrast to AVP,
intravenous infusions of angiotensin II (5, 10, and 50 ng.kg-1.min-1) had
relatively little influence on capacity, whereas norepinephrine
administration (300, 1,000, and 3,000 ng.kg-1.min-1) was associated with
dose-dependent decreases in capacity of 4.5-10.3 ml/kg. Virtually the
entire increase in whole body capacity to AVP can be accounted for by
summation of the predicted contributions of an active reflex venodilatatory
component and those of a passive component (arterial and cardiopulmonary
compartments). Because systemic compliance (delta reservoir volume/delta
venous pressure) was not changed by AVP administration, the contribution of
a reflex venodilatatory component must be the result of increases in
unstressed vascular volume (contained volume at 0 transmural pressure) as
opposed to changes in compliance. These results may explain why AVP
decreases cardiac output to a greater extent than either angiotensin II or
sympathomimetics and, thus, why AVP is a weaker pressor agent in animals
with intact autonomic function.
