Multiple receptor contributions to ovine fetal cardiovascular responses to vasopressin

Selective AVP V1 receptor antagonist and V2 receptor agonist treatments were used to study V1 and V2 receptor contributions to AVP-induced effects on ovine fetal blood pressure, heart rate, and renal function. The results indicate that V1 receptors do not contribute to late gestation fetal renal responses to AVP. The pressor response to AVP was abolished by V1 receptor blockade while the heart rate response was not affected (Fig. 1). This separation of the blood pressure and heart rate responses to AVP has been noted previously, and indicates that AVP-induced fetal bradycardia is not a reflex response to increased blood pressure. A direct V1 receptor-mediated effect on the heart also appears unlikely. The absence of a dDAVP effect on fetal heart rate indicates that AVP-induced bradycardia is not a V2 receptor-mediated event. An AVP effect on oxytocin receptors appears unlikely due to the antioxytocic action of the Manning Compound. Demonstration of AVP V1a receptors in and around the brainstem cardiovascular control centers supports the view that circulating AVP can modulate vagal outflow via effects in the area postrema. However, if Manning Compound infusion blocks fetal V1a receptor-mediated vascular responses and V1b receptor-mediated ACTH release, then blockade of the heart rate response to AVP also would have been expected. In summary, the fetal heart rate response to AVP is not dependent on AVP-induced increases in blood pressure, V1 receptors blocked by the Manning Compound, or V2 receptors stimulated by dDAVP. We conclude that AVP contributes to fetal heart rate regulation, and the effect is not mediated by any known population of AVP receptors.