Mediation by nitric oxide of neurally-induced human cerebral artery relaxation.
Human cerebral artery strips relaxed in response to non-adrenergic, non-cholinergic vasodilator nerve stimulation by electrical pulses or nicotine. The relaxation response was abolished by treatment with NG-nitro-L-arginine, a nitric oxide synthase inhibitor; the inhibitory effect was reversed by L-, but not D-, arginine. Nitric oxide-induced relaxation was unaffected. These findings support the hypothesis that nitric oxide plays a crucial role, possibly as neurotransmitter, in transmitting information from vasodilator nerve to smooth muscle in human cerebral arteries.
Department of Pharmacology, Shiga University of Medical Sciences, Japan.
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Toda
D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D002536:Cerebral Arteries / Q000294:innervation / Q000502:physiology*; D006152:Cyclic GMP / Q000502:physiology; D004558:Electric Stimulation; D006801:Humans; D066298:In Vitro Techniques; D009538:Nicotine / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019335:Nitroarginine; D014664:Vasodilation
D019335:Nitroarginine; D009569:Nitric Oxide; D009538:Nicotine; D001120:Arginine; D006152:Cyclic GMP