EFFECT OF CAROTID DENERVATION ON PLASMA VASOPRESSIN LEVELS DURING ACUTE-HYPOXIA IN THE LATE-GESTATION SHEEP FETUS

1. We measured plasma concentrations of arginine vasopressin (AVP), ar terial, venous and amniotic pressures, and carotid and femoral blood f lows in fifteen chronically instrumented fetal sheep at 119-125 days o f gestation. In eight of the fetuses the carotid sinus nerves were cut (denervated fetuses); the other seven remained intact and served as c ontrols (intact fetuses). 2. In the intact fetuses during hypoxia ther e was an increase in plasma [AVP] and in perfusion (arterial-venous) p ressure, a transient bradycardia, and an increase in carotid and a dec rease in femoral blood flow. Whilst femoral vascular resistance (perfu sion pressure/femoral blood flow) increased, there were no changes in carotid vascular resistance during hypoxia. 3. In the denervated fetus es no significant bradycardia, fall in femoral blood flow or increase in femoral vascular resistance was present soon after the onset of hyp oxia but plasma AVP increased to similar concentrations to those obser ved in intact fetuses during hypoxia. 4. We conclude that carotid dene rvation does not affect plasma [AVP] during hypoxia in fetal sheep. Th is suggests that (1) AVP release during hypoxia is not mediated by a c arotid chemoreflex and (2) AVP does not play an important role in thes e initial fetal cardiovascular responses. Furthermore, we previously r eported that intact fetuses survive acute hypoxia better than denervat ed fetuses following phentolamine treatment, and we believe this to be due to the action of a non-a-adrenergic vasoconstrictor released in p art via a carotid chemoreflex. The present results suggest that this v asoconstrictor is not AVP.