Abstract
Background: Nitric Oxide is a major mediator of enteric nervous system transmission whose role on intestinal transport of electrolytes has also been recently proposed, with conflicting evidence. We had previously shown that Cholera Toxin (CT) could induce secretion in a non contiguous intestinal segment, possibly as a result of enteric nervous system mediated secretion. Aims: 1) to determine whether L-Arginine, as the metabolic precursor of endogenously released Nitric Oxide, affects the transepithelial transport of water and electrolytes in the small intestine. 2) To verify if Nitric Oxide is the mediator of CT-induced secretion in distal intestinal segment. Methods: We utilized in vivo rat perfusion of jejunum and, in another series of experiments, simulataneous but separated perfusion of jejunum and of colon. Results: In vivo luminally added L-Arginine, but not L-Lysine, had a dose-dependent anti-absorptive effect on the jejunal transport of water, Na and Cl. Half-maximal effect is seen at the concentration of 0.05 mM. The addition of Carboxy-PTIO, a known antagonist of free NO, significantly reversed the effect of L-Arginine. When perfused in the jejunum, CT induced a significant shift toward secretion of water and electrolytes both in that segment and in the colon. The presence of carboxy-PTIO in the colon completely abolished this distant secretory effect. Measurement of tissue cyclic nucleotides showed that cGMP concentration is significantly raised by L-Arginine. Conclusions: L-Arginine has a significant secretory effect on small intestinal ion and water transport, and this effect is due to its role as a metabolic precursor of Nitric Oxide and appears to be mediated by elevated cGMP. Furthermore, Nitric Oxide appears to be the mediator of CT-induced secretion in non contiguous intestinal segments.
Published Version
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