role of nitric oxide and atp-sensitive k+ channels in regulation of basal blood flow and hypercapnic vasodilatation of cerebral blood vessels in rabbit

background: the mechanisms underlying cerebral hypercapnic vasodilatation are not fully understood.   objective: to investigate the role of nitric oxide (no) and atp-sensitive potassium (k atp ) channels in basal blood flow regulation and hypercapnia-induced vasodilatation in rabbit cerebral blood vessels.   methods: 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.   results: 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 k atp 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).   conclusion: 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 k atp channels did not mediate the effect of no or other vasodilators responsible for increasing cerebral blood flow during hypercapnia.