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Role of adenosine receptor subtypes in rat jejunum in unfed state versus glucose-induced hyperemia. | LitMetric

AI Article Synopsis

  • Adenosine plays a crucial role in regulating blood flow in the intestines, particularly in how blood vessels react during rest and when glucose is present.
  • The study used video microscopy to observe how two types of blood vessels in rats reacted to adenosine and glucose, showing that smaller arterioles were more responsive to adenosine than larger ones.
  • The research concluded that multiple adenosine receptors (A1, A2a, and A2b) are involved in controlling blood vessel dilation, with the A1 receptor having the most significant impact on glucose-induced vasodilation.

Article Abstract

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 nm), and the A2b receptor antagonist, alloxazine (60 microm), 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 nm) 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.

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Source
http://dx.doi.org/10.1016/j.jss.2006.08.019DOI Listing

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