Cardiovascular effects of vasopressin following V1 receptor blockade compared to effects of nitroglycerin
Department of Medicine, Veterans Affairs Medical Center and University of Tennessee Health Sciences Center, Memphis, Tennessee 38104 Studies to more clearly determine the mechanisms associated with arginine vasopressin (AVP)-induced vasodilation were performed in normal subjects and in quadriplegic...
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Published in | American journal of physiology. Regulatory, integrative and comparative physiology Vol. 281; no. 3; p. 887 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
01.09.2001
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Online Access | Get full text |
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Summary: | Department of Medicine, Veterans Affairs Medical Center and
University of Tennessee Health Sciences Center, Memphis, Tennessee
38104
Studies to more
clearly determine the mechanisms associated with arginine vasopressin
(AVP)-induced vasodilation were performed in normal subjects and in
quadriplegic subjects with impaired efferent sympathetic responses.
Studies to compare the effects of AVP with the hemodynamic effects of
nitroglycerin, an agent that primarily affects venous capacitance
vessels, were also performed in normal subjects. Incremental infusions
of AVP following V 1 -receptor blockade resulted in
equivalent reductions in systemic vascular resistance (SVRI) in normal
and in quadriplegic subjects. However, there were major differences in
the effect on mean arterial pressure (MAP), which was reduced in
quadriplegic subjects but did not change in normal subjects. This
difference in MAP can be attributed to a difference in the
magnitude of increase in cardiac output (CI), which was twofold greater
in normal than in quadriplegic subjects. These observations are
consistent with AVP-induced vasodilation of arterial resistance vessels
with reflex sympathetic enhancement of CI and are clearly different
from the hemodynamic effects of nitroglycerin, i.e., reductions in MAP,
CI, and indexes of cardiac preload, with only minor changes in SVRI.
vasopressin 1-receptor antagonist; hemodynamic effects |
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ISSN: | 0363-6119 1522-1490 |
DOI: | 10.1152/ajpregu.2001.281.3.r887 |