Role of Adenosine Receptor Subtypes in Rat Jejunum in Unfed State Versus Glucose-Induced Hyperemia

• Published in: The Journal of surgical research 2007-05, Vol.139 (1), p.51-60
• Main Authors: Li, Na, M.D., Ph.D, Harris, Patrick D., Ph.D, Zakaria, El Rasheid, M.D., Ph.D, Matheson, Paul J., Ph.D, Garrison, R. Neal, M.D
• Format: Article
• Language: English
• Subjects: adenosine; Adenosine - pharmacology; Animals; Arterioles - drug effects; Arterioles - physiology; Biological and medical sciences; Blood Pressure; D-glucose; Dose-Response Relationship, Drug; General aspects; Glucose - pharmacology; Heart Rate; Hyperemia - physiopathology; Jejunum - blood supply; Male; mannitol; Medical sciences; microvessels; postprandial hyperemia; purinergic receptors; Rats; Rats, Sprague-Dawley; Receptors, Purinergic P1 - classification; Receptors, Purinergic P1 - physiology; Surgery; Vasodilation - drug effects
• ISSN: 0022-4804; 1095-8673
• DOI: 10.1016/j.jss.2006.08.019

Background Adenosine is a key mediator in intestinal absorptive hyperemia. This study examines the role of adenosine receptor subtypes in the intestinal microvasculature at rest (unfed) and during glucose exposure. Materials and methods Intravital video microscopy was used to record vascular responses in the rat jejunum in unfed resting states versus active glucose absorption. Two series of experiments were performed: topical adenosine alone and with adenosine receptor antagonists, and topical glucose alone and with adenosine receptor antagonists. Results We found that distal premucosal arterioles were more reactive to adenosine than were larger inflow arterioles. The selective A1 adenosine receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) (200 n m ), and the A2b receptor antagonist, alloxazine (60 μ m ), decreased the sensitivity and reactivity of the inflow and premucosal arterioles to adenosine, whereas the selective A2a receptor antagonist 8-(3-chlorostyryl)caffeine (CSC) (200 n m ) had no effect on inflow arteriole diameter and only slightly reduced the premucosal arteriolar sensitivity to adenosine. As previously observed, isotonic glucose caused vasodilation (24 ± 3.4% of the control) in the distal premucosal arterioles. Conversely, premucosal arterioles did not dilate during exposure of the intestine to isotonic mannitol solution that is not actively absorbed. Adenosine A2a RA CSC and A2b RA alloxazine attenuated glucose-induced vasodilation, whereas adenosine A1 RA DPCPX completely abolished glucose-induced dilation. Conclusions These findings suggest that resting tone in premucosal vessels appears to be responsive to adenosine mediation rather than inflow arteriolar tone; the adenosine A1, A2a, and A2b receptors all contribute to adenosine-mediated vasodilation in the intestine, with the greatest attenuation seen with A1 receptor antagonism; and other vasoactive mediators might also contribute to glucose-induced jejunal vasodilation, and interaction might exist between adenosine receptors and other mediators.