Adenosine's role in hypercapnia-evoked cerebral vasodilation in the rat.

摘要

Carbon dioxide induces a rapid dilation of cerebral arterioles, enabling local blood flow to match increasing metabolic requirements of tissue. Amongst the vasodilatory substances released by cortical tissue in response to CO2 are adenosine and nitric oxide. Here we report that selective adenosine A(2A) receptor antagonists, applied topically using a rat cortical window technique, significantly depressed the CO2-evoked increase in arteriolar diameter, measured using video microscopy, as well as attenuating the CO2 and pH reactivity of the cortical arterioles. Two non-selective inhibitors of nitric oxide synthase also significantly depressed the hypercapnia-evoked increase in arteriolar diameter.