ARGININE-VASOPRESSIN MODULATION OF ARTERIAL BAROREFLEX RESPONSES IN FETAL AND NEWBORN SHEEP

The present study was designed to test the hypothesis that the influen ce of circulating vasopressin (AVP) on the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) change s during development. To test this hypothesis, we studied arterial bar oreflex-mediated control of HR and RSNA in the presence of increasing plasma levels of AVP in conscious, chronically instrumented fetal, new born, and adult sheep. In fetal and newborn sheep, increasing plasma A VP levels (from <10 to >200 mu U/ml) increased resting levels of mean arterial blood pressure (MABP) and decreased HR and RSNA. HR and RSNA baroreflex responses to variations of MABP with nitroprusside and phen ylephrine infusion were not modified by elevated AVP levels in either newborn or fetal sheep, except for a small decrease in maximal HR resp onse to nitroprusside infusion in the newborn animals. In contrast, in adults, AVP caused bradycardia and a decrease in RSNA without change in MABP, accompanied by resetting of the arterial baroreflex (decrease in maximal HR and RSNA, decrease in RSNA gain, and shift of HR to low er pressure). To test the hypothesis that the inability of AVP to rese t the arterial baroreflex early during development was not secondary t o maximal stimulation of V-1 receptors during baseline conditions, we investigated the effect of V-1-receptor blockade on baseline cardiovas cular and arterial baroreflex function in newborn lambs. Administratio n of a V-1-receptor antagonist produced no significant changes in rest ing MABP, HR, and RSNA and did not influence arterial baroreflex-media ted changes in HR and RSNA. These results indicate that, contrary to a dults, circulating AVP does not modulate the arterial baroreflex in fe tal and newborn sheep.