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1 Department of Surgery, University of Maryland, Baltimore, Maryland 21201; and 2 National Aeronautics and Space Administration, Ames Research Center, Moffett Field, California 94035
We have
proposed that the reflex increase in arginine vasopressin (AVP)
secretion in response to hypovolemia is due to arterial baroreceptor
unloading. If arterial pressure is the key to the mechanism, the slope
relating plasma AVP to arterial pressure should be the same in response
to hemorrhage, a model of true hypovolemia, and in response to thoracic
inferior vena caval constriction (IVCC), a model of central
hypovolemia. We tested this hypothesis in conscious, chronically
instrumented dogs (n = 8). The mean coefficient of
determination (r2) values obtained from the
individual regressions of log AVP onto systolic pressure (SP) and mean
arterial pressure (MAP) in response to hemorrhage were 0.953 ± 0.009 and 0.845 ± 0.047, respectively. Paired
comparisons indicated a significant difference between the means
(P < 0.05), hence, SP was used in subsequent analyses. The mean slopes relating the log of plasma AVP to SP in response to
hemorrhage and IVCC were
0.034 ± 0.003 and
0.032 ± 0.002, respectively, and the means were not significantly different
(P = 0.7). The slopes were not altered when the
experiments were repeated during acute blockade of cardiac receptors by
intrapericardial procaine. Finally, sinoaortic denervation
(n = 4) markedly reduced the slope in both the
hemorrhage and IVCC treatments. We conclude that baroreceptors
monitoring arterial pressure provide the principal reflex control of
AVP secretion in response to hypovolemia.
antidiuretic hormone; arterial baroreceptors; cardiac receptors; atrial receptors; ventricular receptors; blood volume; blood pressure
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