The 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 µmol/l) or adenosine (0.01-10 µmol/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 µmol/l). The vasodilation to cAMP (1-100 µmol/l), adenosine (0.01-10 µmol/l), and hypotension was significantly reduced by pretreatment with 3,7-dimethyl-1-propargylxanthine (1 µmol/l), an A₂ receptor antagonist, as well as 3-isobutyl-1-methylxanthine (3 µmol/l), an inhibitor of endo- and ectophosphodiesterase, 1,3-dipropyl-8-p-sulfophenylxanthine (100 µmol/l), an inhibitor of ecto-5'-phosphodiesterase, or ,-methylene-adenosine 5'-diphosphate (100 µmol/l), an inhibitor of ecto-5'-nucleotidase. However, 8-cyclopentyltheophylline (1 µmol/l), an A₁ antagonist, did not elicit a similar response. The increased release of adenosine when the cortical surface was suffused with cAMP (100 µmol/l) was significantly reduced by 3-isobutyl-1-methylxanthine, 1,3-dipropyl-8-p-sulfophenylxanthine, and ,-methylene-adenosine 5'-diphosphate (each 100 µmol/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.

A₁ and A₂ receptors; cerebral autoregulation; calcitonin gene-related peptide

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