Role of nitric oxide in the coupling of cerebral blood flow to neuronal activation in rats.
We tested the hypothesis that nitric oxide (NO) is a mediator in the coupling of cerebral blood flow to neuronal activation. The production of NO was blocked in anesthetized rats with the NO-synthase inhibitor N omega-nitro-L-arginine (L-NA). In controls, vibrissae stimulation for 60 s led to a fast (< or = 2 s), 17% increase in regional cerebral blood flow (rCBF) in the contralateral somatosensory cortex. Systemical (10 mg/kg) as well as topical (10(-3) M) application of L-NA reduced the response to stimulation by approximately 50%. Systemical application primarily attenuated the early component of the response, whereas topical application led to an attenuation throughout the whole 60-s stimulation interval. We conclude that NO is involved in rCBF coupling to neuronal activation.
Dirnagl
U
U
Department of Neurology, Klinikum Grosshadern, Munich, FRG.
Lindauer
U
U
Villringer
A
A
D000287:Administration, Topical; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D007275:Injections, Intravenous; D008297:Male; D009474:Neurons / Q000502:physiology*; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019335:Nitroarginine; D010812:Physical Stimulation; D051381:Rats; D017208:Rats, Wistar; D013003:Somatosensory Cortex / Q000098:blood supply; D014738:Vibrissae / Q000502:physiology
D019335:Nitroarginine; D009569:Nitric Oxide; D001120:Arginine