Abstract
The effect of intravenous injection of nicotine on cortical cerebral blood flow (CBF) was examined in urethane anesthetized rats. Nicotine (3–30 μg/kg) increased cortical CBF, independent of mean arterial pressure. This response was attenuated to about a half of the control one after lesioning the nucleus basalis of Meynert (NBM) bilaterally. The response was not significantly influenced after blocking the muscarinic receptors, but was abolished after blocking the nicotinic receptors in the parenchyma of the brain. It is concluded that the nicotine-induced cortical vasodilation was mediated by activation of the nicotinic receptors in the NBM and also in the cortex of the brain. The threshold dose of nicotine for increasing cortical CBF was shifted in aged rats of 23–26 months, and the nicotine-induced increase in cortical CBF was much reduced in aged rats of 32–36 months. Activation of nicotinic receptors in the brain may be of therapeutic value in aged subjects in facilitating the cholinergic neural vasodilative system.
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