THE ROLE OF THE AUTONOMIC NERVOUS SYSTEM IN THE RESPONSES OF THE PERFUSED CANINE PAW TO PROSTAGLANDINS B1 AND B2

The interaction between the autonomic nervous system and prostaglandin B2 (PGB2) and prostaglandin B1 (PGB1)-induced vasoconstriction was evaluated in the normally innervated and acutely denervated canine hindpaw perfused with autologous blood at constant flow. Intra-arterial infusions of PGB2 (50-1600 ng/kg/min) produced concentration-dependent vasoconstriction. Pretreatment of dogs with bretylium (20 mg/kg i.v.), phentolamine (2 mg/kg i.v.), reserpine (0.5 mg/kg/day for 2 days) or acute denervation unmasked a vasodilator component to PGB2 and reduced the magnitude of the constrictor response to this prostaglandin. However, the constrictor response to PGB2 could not be abolished by adrenergic blocking agents. In contrast to these findings, low concentrations of PGB1 (50-200 ng/kg/min) dilated the canine hindpaw whereas higher concentrations (200-3200 ng/kg/min) resulted in cutaneous vasoconstriction. PGB1 is 8 times less potent a vasoconstrictor than PGB2. Bretylium and phentolamine, reserpine and acute denervation also reduced the vasoconstrictor response to PGB1. These findings suggest that 1) PGB2 and PGB1 act directly on smooth muscle to cause both vasodilation and vasoconstriction, 2) a portion of the vasoconstrictor respouse to these prostaglandins is mediated by PGB-induced release of catecholamines from adrenergic nerve terminals and 3) PGB-induced release of catecholamines appears to be dependent on the electrical impulse activity along the sympathetic adrenergic fibers.