Rectal distention-induced colonic net water secretion in rats involves tachykinins, capsaicin sensory, and vagus nerves.

Abstract

Distention of the intestine induces neural anion secretion in vitro. Both substance P and neurokinin A modify water and ion transport in vivo. This study investigated in vivo (1) the effect of rectal distention (RD) on proximal colonic net water flux, (2) the role of tachykinins, and muscarinic and nicotinic connections, and (3) the influence of capsaicin-sensitive nerves and vagotomy in this effect. In anesthetized rats, colonic loops were infused with [14C]polyethylene glycol 4000 Ringer's buffer. Net water flux was calculated according to 14C activity in the effluent collected. RD was performed by inflation of a balloon (2 mL) in the rectum. RD induced a colonic net water hypersecretion. This effect was blocked by previous systemic capsaicin, vagotomy, atropine, and hexamethonium treatment. Both neurokinin 1 (NK1) (SR-140,333; 1 mg/kg) and NK2 (MEN-10,627; 150 microg/kg) antagonists administered intraperitoneally suppressed the RD-hypersecretory effect, whereas NK2 (MEN-10,627; 1.5 microg/kg) and NK3 (SR-142,801; 0.01 mg/kg) antagonists are active when injected intracerebroventricularly. In vivo, RD induces colonic net water secretion in rats, involving capsaicin-sensitive innervation and vagal nerves. This effect involves tachykininergic pathways at both peripheral and central levels.