Arginine vasopressin modulation of arterial baroreflex responses in fetal and newborn sheep.

Abstract

The present study was designed to test the hypothesis that the influence of circulating vasopressin (AVP) on the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) changes during development. To test this hypothesis, we studied arterial baroreflex-mediated control of HR and RSNA in the presence of increasing plasma levels of AVP in conscious, chronically instrumented fetal, newborn, and adult sheep. In fetal and newborn sheep, increasing plasma AVP levels (from < 10 to > 200 microU/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 phenylephrine infusion were not modified by elevated AVP levels in either newborn or fetal sheep, except for a small decrease in maximal HR response 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 lower pressure). To test the hypothesis that the inability of AVP to reset the arterial baroreflex early during development was not secondary to maximal stimulation of V1 receptors during baseline conditions, we investigated the effect of V1-receptor blockade on baseline cardiovascular and arterial baroreflex function in newborn lambs. Administration of a V1-receptor antagonist produced no significant changes in resting MABP, HR, and RSNA and did not influence arterial baroreflex-mediated changes in HR and RSNA. These results indicate that, contrary to adults, circulating AVP does not modulate the arterial baroreflex in fetal and newborn sheep.