VASOPRESSIN, RENIN, AND CORTISOL RESPONSES TO HEMORRHAGE DURING ACUTEBLOCKADE OF CARDIAC NERVES IN CONSCIOUS DOGS

The effect of acute cardiac nerve blockade (CNB) on the increases in p lasma renin activity (PRA), arginine vasopressin (AVP), and cortisol i n response to a 30 ml/kg hemorrhage was determined in conscious dogs ( n = 9). Procaine was infused into the pericardial space to produce acu te reversible CNB, or saline was infused in the control hemorrhage. Bl ood was removed from the inferior vena cava at a rate of 1 ml.kg-1.min -1. In the control hemorrhage, plasma AVP increased from 1.8 +/- 0.3 t o 219 +/- 66 pg/ml, PRA increased from 0.63 +/- 0.20 to 3.08 +/- 0.91 ng angiotensin I (ANG I).ml-1.3 h-1, and cortisol increased from 1.4 /- 0.2 to 4.0 +/- 0.7 mug/dl. When the hemorrhage was repeated during acute CNB, plasma AVP increased from 2.8 +/- 1.6 to 185 +/- 59 pg/ml, PRA increased from 0.44 +/- 0.14 to 2.24 +/- 0.27 ng ANG I.ml-1.3 h-1, and cortisol increased from 1.9 +/- 0.3 to 5.4 +/- 0.6 mug/dl, and no ne of the increases differed significantly from the responses during t he control hemorrhage. Left atrial pressure fell significantly after r emoval of 6 ml/kg of blood, but mean arterial pressure was maintained at control levels until blood loss reached 20 ml/kg during pericardial infusion of either saline or procaine. The declines in MAP at the 30 ml/kg level of hemorrhage in both treatments were similar. These resul ts demonstrate that acutely blocking input from cardiac receptors does not reduce the increases in plasma AVP, cortisol, and PRA in response to a 30 ml/kg hemorrhage. The results of this study do not support th e hypothesis that input from cardiac receptors is required for a norma l AVP response to hemorrhage and suggest that other receptors, presuma bly arterial baroreceptors, can stimulate AVP and cortisol secretion i n the absence of signals from the heart.