Systolic pressure predicts plasma vasopressin responses to hemorrhage and vena caval constriction in dogs

We have proposed that the reflex increase in arginine vasopressin (AVP) sec retion in response to hypovolemia is due to arterial baroreceptor unloading . If arterial pressure is the key to the mechanism, the slope relating plas ma 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 hypoth esis in conscious, chronically instrumented dogs (n = 8). The mean coeffici ent of determination (r(2)) 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, respectiv ely. Paired comparisons indicated a significant difference between the mean s (P< 0.05), hence, SP was used in subsequent analyses. The mean slopes rel ating 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 exp eriments were repeated during acute blockade of cardiac receptors by intrap ericardial procaine. Finally, sinoaortic denervation (n = 4) markedly reduc ed the slope in both the hemorrhage and IVCC treatments. We conclude that b aroreceptors monitoring arterial pressure provide the principal reflex cont rol of AVP secretion in response to hypovolemia.