Abstract
Our goals were to determine whether acute exposure to nicotine alters eNOS‐dependent responses of the basilar artery and to identify a potential role for activation of NAD(P)H oxidase. We measured diameter of the basilar artery to eNOS‐dependent (acetylcholine) and ‐independent (nitroglycerin) agonists before and during acute infusion of nicotine in the absence or presence of apocynin. In addition, we measure superoxide production by brain tissue to nicotine. We found that eNOS‐dependent vasodilatation was impaired during treatment with nicotine and that apocynin prevented this impairment. Further, the production of superoxide was increased by nicotine and this increase could be inhibited by apocynin. We suggest that nicotine impairs eNOS‐dependent dilatation of the basilar artery by activation of NAD(P)H oxidase.
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