Central nervous system influence of prostaglandin E2 on jejunal water and electrolyte transport in conscious dogs

Abstract

The effects of intracerebroventricular (i.c.v.) vs. i.v. administration of prostaglandin E2 (PGE2) on net fluxes of water, Na+, and K+ through a jejunal Thiry-Vella loop were investigated before or after previous treatment with adrenergic blockers, indomethacin, and 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB8) in conscious dogs. Administered intracerebroventricularly at doses of 20–100 ng/kg, PGE2 significantly reduced (p < 0.01), in a dose-related manner, the net fluxes of water, Na+, and K+, which were reversed from an absorption to a secretion. Intravenously administered PGE2 at a five times higher dosage failed to significantly alter net water and electrolyte fluxes. Phentolamine (0.2 mg/kg body wt) and tolazoline (2 mg/kg body wt) administered intravenously abolished the secretory effects of centrally administered PGE2 (50 ng/kg). However, 10 times lower dosages of phentolamine and tolazoline administered intracerebroventricularly did not prevent the PGE2-induced secretion of water and electrolytes. Intracerebroventricular administration of indomethacin (10 μg/kg body wt) and TMB8 (1 μg/kg body wt), did not modify the effect of i.c.v.-administered PGE2; however, indomethacin administered intracerebroventricularly alone stimulated water and electrolyte absorption. None of these treatments results in a significant (p > 0.05) change in mean transit time through the Thiry-Vella loop. We conclude that centrally administered PGE2 influences jejunal water, Na+, and K+ absorption, through a mechanism related to adrenergic innervation and/or involving at least α2-adrenoceptors. The results also suggest that PGE2 in the central nervous system controls jejunal water and ion transport in the dog.