Central and reflexogenic cardiovascular actions of prostaglandin E1

The centrally mediated cardiovascular effects of prostaglandin E₁ (PGE₁) were investigated using cross-circulation procedures. PGE₁ was injected into the arterial inflow (IA-R) of vascularly isolated, ncurally intact heads of anesthetized recipient dogs. Following the administration of 5 and 10 μg/kg of PGE₁ (IA-R) consistent depressor responses occurred in the donor dogs and in the recipient's isolated trunk. The administration of 5 and 10 μg/kg of PGE₁ (IA-R) to debuffered recipients (carotid sinus-body areas bilaterally denervated) elicited centrally mediated pressor responses in the recipient's trunk paralleled by depressor effects in the donor and a decline in the recipient's perfusion pressure. Centrally mediated pressor responses of angiotensin II were inhibited by PGE₁ only in the non-debuffered recipients. Pressor responses to PGE₁ in debuffcrcd recipients were blocked by the ganglionic blocking agent, hexamethonium. These data plus results from the intra-artcrial administration of PGE₁ into the carotid sinus area before and after denervation suggest that the carotid sinusbody structures, most likely the baroreceptors, are primarily implicated in the hypotensive response to PGE₁ in the non-debuffered recipient's trunk. On the other hand, the central nervous systemper se appears to be involved in mediation of the central pressor responses obtained in the debuffered preparations. This study provides evidence for the involvement of the carotid sinus-body structures and the central nervous system as additional loci for the cardiovascular effects of PGE₁.