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pubmed-article:9950836pubmed:abstractTextThe purpose of this experiment was to examine whether the cAMP-adenosine pathway is implicated in the autoregulatory vasodilation in response to hypotension. Suffusion with cAMP (1-100 micromol/l) or adenosine (0.01-10 micromol/l) caused a sustained vasodilation of the resting pial arteries in a concentration-dependent manner. In contrast, N6,2'-O-dibutyryl-cAMP and 8-bromo-cAMP exerted a weak dilation at high concentration (100 micromol/l). The vasodilation to cAMP (1-100 micromol/l), adenosine (0.01-10 micromol/l), and hypotension was significantly reduced by pretreatment with 3,7-dimethyl-1-propargylxanthine (1 micromol/l), an A2 receptor antagonist, as well as 3-isobutyl-1-methylxanthine (3 micromol/l), an inhibitor of endo- and ectophosphodiesterase, 1, 3-dipropyl-8-p-sulfophenylxanthine (100 micromol/l), an inhibitor of ecto-5'-phosphodiesterase, or alpha,beta-methylene-adenosine 5'-diphosphate (100 micromol/l), an inhibitor of ecto-5'-nucleotidase. However, 8-cyclopentyltheophylline (1 micromol/l), an A1 antagonist, did not elicit a similar response. The increased release of adenosine when the cortical surface was suffused with cAMP (100 micromol/l) was significantly reduced by 3-isobutyl-1-methylxanthine, 1,3-dipropyl-8-p-sulfophenylxanthine, and alpha,beta-methylene-adenosine 5'-diphosphate (each 100 micromol/l). These results indicate that the cAMP-adenosine pathway as a viable metabolic mechanism is implicated in the production of adenosine in the rat pial artery and contributes to the regulation of vasodilation in response to hypotension.lld:pubmed
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pubmed-article:9950836pubmed:authorpubmed-author:ShinH KHKlld:pubmed
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pubmed-article:9950836pubmed:dateRevised2010-11-18lld:pubmed
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pubmed-article:9950836pubmed:articleTitleMetabolism of cAMP to adenosine: role in vasodilation of rat pial artery in response to hypotension.lld:pubmed
pubmed-article:9950836pubmed:affiliationDepartment of Pharmacology, College of Medicine, Pusan National University, Pusan 602-739, Korea.lld:pubmed
pubmed-article:9950836pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9950836pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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