Glucose and glutamine gavage increase portal vein nitric oxide metabolite levels via adenosine A2b activation

Introduction. Postprandial intestinal hyperemia is a complex vascular respo nse during nutrient absorption. Many mediators have been studied including enteric reflexes, GI hormones, and absorption-stimulated metabolic mediator s such as pH and adenosine. We have shown that nitric oxide (NO) mediates p remucosal arteriolar dilation during glucose absorption and that glucose-in duced portal vein NO metabolite production requires adenosine A2b receptor activation. We hypothesize that Na+-linked absorption of L-glutamine or L-g lycine might also stimulate NO release in the enteroportal circulation via adenosine A2b receptors. Methods. Male Sprague-Dawley rats (190-220 g) were anesthetized with uretha ne/alpha-chloralose and cannulated for hemodynamic monitoring and blood sam pling. A right paramedian abdominal incision was made for access to both th e stomach (gavage) and the portal vein (blood sampling). Animals received i ntragastric nutrient gavage (saline, D-glucose, L-glutamine, racemic glycin e, or oleic acid) with and without adenosine A2b receptor blockade. NO meta bolites (NOx) were measured by a fluorescent modified-Greiss assay at basel ine and 30 min after nutrient gavage. Results. Glucose and glutamine gavage increased portal NOx levels compared to baseline, while glycine and oleic acid gavage did not. Adenosine A2b ant agonism returned NOx levels to baseline in both glucose and glutamine gavag e animals, but did not alter portal NOx levels in glycine- or oleic acid-tr eated animals. Conclusions. These data suggest that nutrient-indnced adenosine is involved in a signaling process from the intestinal epithelium to nitric oxide-prod ucing cells elsewhere in the vasculature. Adenosine A2b receptors are requi red for NO production during Na+-linked glucose or glutamine absorption. (C ) 1999 Academic Press.