Role of Nitric Oxide and ATP-Sensitive K+ Channels in Regulation of Basal Blood Flow and Hypercapnic Vasodilatation of Cerebral Blood Vessels in Rabbit

The mechanisms underlying cerebral hypercapnic vasodilatation are not fully understood. To investigate the role of nitric oxide (NO) and ATP-sensitive potassium (KATP) channels in basal blood flow regulation and hypercapnia-induced vasodilatation in rabbit cerebral blood vessels. The change in cerebral blood flow was measured by a laser Doppler flowmeter in 18 New Zealand white rabbits, in two groups, under general anesthesia with sodium pentobarbital. N-omega-nitro-L-arginine methyl ester (L-NAME) and glibenclamide were administered locally and systemically before and during induction of hypercapnia. The change in cerebral blood flow was not significant following local and systemic L-NAME administration, showing a non-significant role of local and systemic NO in regulation of rabbit basal cerebral blood flow. Hypercapnia increased cerebral blood flow by 17.3±4.4% before and 17.3±5.8% after local, and 5.8±3.2% (p<0.05) after systemic L-NAME administration. The change in cerebral blood flow was not significant after local and systemic administration of glibenclamide indicating a lack of KATP channel role in basal blood flow regulation. Hypercapnia increased cerebral blood flow by 27.2±8.7% before and 24.7±6.4% after local, and 49.3±9.7% after systemic administration of glibenclamide (p: NS in both cases). Regional NO production had no role in basal cortical blood flow regulation and systemic NO contributed to 66% increment in cerebral blood flow during hypercapnia. Also, the KATP channels did not mediate the effect of NO or other vasodilators responsible for increasing cerebral blood flow during hypercapnia.