L-arginine prevents impaired endothelium-dependent cerebral arteriolar dilatation during acute infusion of nicotine.

Exogenous treatment with L-arginine has been shown to restore impaired nitric oxide synthase (NOS)-dependent dilatation of peripheral blood vessels during disease states. We have shown that nicotine impairs NOS-dependent arteriolar dilatation in the cerebral circulation. However, the role of L-arginine in impaired responses of cerebral arterioles during infusion of nicotine has not been examined. Thus the goal of the present study was to examine the role of L-arginine in nicotine-induced impairment of cerebral arteriolar reactivity. We measured the diameter of pial arterioles in response to NOS-dependent (5'-adenosine diphosphate [ADP] and acetylcholine) and NOS-independent (nitroglycerin) agonists before and after infusion of vehicle or nicotine (2 microg/kg/min intravenously for 30 min followed by a maintenance dose of 0.35 microg/kg/min) in the absence or presence of L-arginine (10(-3) M). We found that topical application of L-arginine to cerebral microvessels during infusion of nicotine could prevent impaired NOS-dependent vasodilatation. We suggest that exogenous L-arginine may have a beneficial role in preventing cerebral microvascular dysfunction during exposure to nicotine.