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The Involvement of Nitric Oxide and Guanylate Cyclase on the Adenosine A2B Receptor-induced Cerebral Blood Responses in the Rats  

Park, Chan-Sook (Department of Pharmacology, College of Medicine, Hanyang University)
Shin, In-Chul (Department of Pharmacology, College of Medicine, Hanyang University)
Publication Information
Biomolecules & Therapeutics / v.13, no.2, 2005 , pp. 95-100 More about this Journal
Abstract
This study was performed to investigate the mechanism of cerebral blood flow of adenosine $A_{2B}$ receptor agonist in the rats, and to define whether its mechanism is mediated by nitric oxide (NO) and guanylate cyclase. In pentobarbital-anesthetized, pancuronium-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood flow from cerebral cortex was measured using laser-doppler flowmetry. Topical application of an adenosine $A_{2B}$ receptor agonist, 5'-N-ethylcar-boxamidoadenosine (NECA; $4{\mu}mol/l$) increased cerebral blood flow. This effect of NECA ($4{\mu}mol/l$) was blocked by pretreatment with NO synthase inhibitor, $N^G$-nitro-L-argine methvlester (L-NAME; $40{\mu}mol/l$) and guanylate cyclase inhibitor, LY-83,583 ($10{\mu}mol/l$). These results suggest that adenosine $A_{2B}$ receptor increases cerebral blood flow. It seems that this action of adenosine $A_{2B}$ receptor is mediated via the NO and the activation of guanylate cyclase in the cerebral cortex of the rats.
Keywords
5'-N-ethylcarboxamidoadenosine; cerebral blood flow; nitric oxide; guanylate cyclase;
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