The goal of these experiments was to determine the presence and mechanistic basis of flow-induced dilation in mesenteric artery from 3-d-old swine. In the first experiment, in vitro gut loops were perfused from a blood-filled reservoir under controlled-flow conditions, and flow was progressively increased from~40 % to~170% in six increments by manipulation of pump speed. Under control conditions, vascular resistance significantly decreased after each step increase in flow rate. WMonomethyl-t-arginine (LNMMA; 10-4 M), an arginine analog that blocks nitric oxide production, eliminated this flow-induced dilation, but only for the step increases in flow at rates above the baseline flow rate. For step increases below the baseline rate, LNMMA caused a simple parallel shift of the resistance-flow rate curve upward. Phenylephrine (10-6 M), an (X l-agonist which has no effect on nitric oxide production or half-life, did not eliminate flow-induced dilation, but instead caused a simple parallel shift of the resistance-flow rate curve upward across the entire range of flows studied. In the second experiment, a 3-cm segment of mesenteric artery was perfused with Krebs buffer at two flow rates: 10 and 25 mU min. The effluent from the rnesFlow-induced dil ation is a vascular phenomenon wh erein aug me ntation of flow rate throu gh an art ery res ults in vasodilation of that ves sel (1). Th e proc ess was init iall y described in large conduit arteries and was presumed to be part of series of va scular adjustments which facilitate oxygen delivery during exercise (1, 2). In this sce nario, resistance vessels within the microcir cul ation of co ntrac ting muscle dil ate in response to a metaboli c feedb ack signal, an action which decre ases downstrea m vascular resista nce. This hemodynamic ch ange increases flow rate throu gh the co nduit ves se ls leading to the mu scl e. Th e stimulus of inc reas ed flow rate induces dil ation of the conduit vessels, an action which maximizes vascular conduct ance . Subsequent studies hav e identified flow-induced dilation within arterioles (3) and have establ ish ed that flowinduced dil ation is an endo thelium-dependent process, that is, enteric artery segment was suffused onto a deendothelialized, phenylephrine-precontracted ring of swine carotid artery; relaxation of this bioassay vessel served as an index of release of relaxing factors from the mesenteric artery segment. Under control conditions, increase in the mesenteric artery flow rate caused a 60% relaxation of the bioassay vessel. This effect was eliminated by the addition of LNMMA to the buffer (10-4 M), but not by the addition of indomethacin (10-5 M). Flow-induced dilation occurs in the mesenteric artery of 3-d-old swine. This vascular phenomenon appears to be mediated by nitric oxide, but only at flows above the baseline flow rate. The mechanism(s) responsible for this phenomenon at lower flow rates is not clear. (Pediatr Res 38: 783-791, 1995) Abbreviations NO, nitric oxide LNMMA, W-monomethyl-i. -arginine (a-v)02' arteriov...