Baroreflex control of plasma arginine vasopressin in humans.

We postulated an interaction between the osmoreceptor and baroreceptor regulation of arginine vasopressin (AVP) release in humans such that the modulating effects of the baroreceptors on AVP release may be undetectable unless the serum osmolality is elevated. We studied normal subjects in both a water-replete (WR, n = 9) and water-deplete (WD, n = 9) state. We monitored blood pressure, central venous pressure, and forearm blood flow. In both WR and WD subjects selective unloading of cardiac baroreceptors with lower body negative pressure (LBNP) -15 mmHg for 30 min did not increase AVP levels. Combined unloading of cardiac and arterial baroreceptors by LBNP -40 mmHg for 10 min significantly increased AVP levels in only the fluid-deplete group [3.54 +/- 0.40 to 8.09 +/- 1.40 (SE) microU/ml, control vs. LBNP -40 mmHg, P less than 0.05]. Mean arterial pressures did not decrease with LBNP -40 mmHg for 10 min. Further analysis of the data based on serum osmolalities (OSM) indicated that LBNP -40 mmHg significantly increased AVP levels (3.72 +/- 0.43 to 13.59 +/- 3.63 microU/ml; P less than 0.05; n = 9) during sessions with OSM greater than 294 mosmol/kg, but not during sessions with OSM less than 294 mosmol/kg (2.85 +/- 0.29 to 4.66 +/- 1.15 microU/ml; P = NS; n = 11). This study demonstrates that significant baroreflex-mediated regulation of vasopressin can occur in humans in the absence of overt hypotension. Second, it reveals an interaction between osmoreceptor and baroreceptor regulation of vasopressin levels in humans such that physiological unloading of cardiac and arterial baroreceptors significantly increases plasma vasopressin levels only when serum osmolality is increased.