ACTIVE REFLEX VASODILATATION INDUCED BY INTRAVENOUS EPINEPHRINE OR NOREPINEPHRINE IN PRIMATES

The hindquarters of rhesus and vervet monkeys were perfused at constant flow. Changes in vascular resistance were determined from the perfusion pressure. Intravenous injection of epinephrine or norepinephrine produced a rise in systemic blood pressure and a concomitant reflex vasodilatation in the innervated hindquarters. This reflex vasodilatation was reduced or abolished by sympathetic decentralization. A component of the dilatation was active ( i.e., due to the discharge of sympathetic vasodilator fibers) because the minimum perfusion pressure reached during the nadir of reflex dilatation elicited before decentralization was significantly lower than the sustained level in perfusion pressure after decentralization. Neither adrenalectomy, beta adrenergic blocking agents nor atropine decreased the reflex dilatation. In contrast. tripelennamine produced an equivalent reduction of both reflex and histamine-induced dilatation. It is concluded that a component of pressoreceptor-induced reflex dilatation is mediated in monkeys by the neurogenic release of histamine, as shown previously for dogs. Both active and passive components of the reflex are mediated over the sympathetic nervous system.