Evidence and quantification of the vasopressin arterial pressure control system in the dog.

Abstract

The recovery of arterial pressure after rapid hemorrhage was studied in 10 dogs with spinal cord destruction below the level of C-1 to remove efferent sympathetic nerve activity. Bilateral nephrectomy was used to remove the renin-angiotensin system. Results for this group were compared to those for another group of dogs in which the entire CNS, including the pituitary gland, were removed surgically. In all groups, arterial pressure was lowered rapidly from an average control value of 106 .+-. 2 (mean .+-. SE) to 51 .+-. 1 mm Hg by hemorrhage. In dogs with spinal cord destruction and bilateral nephrectomy, arterial pressure rose from 51 mm Hg to 89 .+-. 3 mm Hg in 3 min and stabilized at that level over the next 30 min, representing a 71% compensation of arterial pressure. Left atrial pressure fell from 3.3 to 0.8 mm Hg during hemorrhage and subsequently rose only 12% during the hemorrhage. Plasma AVP [Arg vasopressin] rose during hemorrhage from 19 .+-. 2 to 75 .+-. 10 .mu.U[units]/ml. Injection of the competitve AVP inhibitors, [1-deaminopenicillamine, 4-valine]-8-D-arginine-vasopressin (dPVDAVP), completely reversed the effects and returned the compensated pressure to 50 mm Hg. In the complete absence of CNS, arterial pressure compensation averaged only 10 .+-. 3%. Plasma osmolality, Na and K concentrations, hematocrit and heart rate were unchanged in all experimental groups. The relationships involved in the AVP-arterial pressure control system were determined quantitatively and analyzed. A systems analysis using experimentally determined values for AVP secretion and metabolism, plasma AVP and changes in arterial pressure closely predicted the changes observed during hemorrhage. AVP apparently has potent systemic vasoconstrictor actions enabling it to make a significant contribution in the restoration of arterial pressure during hemorrhage.