Neural regulation of blood flow in the rat submandibular gland

Blood flow in salivary glands is regulated mainly by sympathetic and parasympathetic nerve activity. This study was carried out to determine the relative contributions of cholinergic, adrenergic and peptidergic neurotransmitters to the control of submandibular blood flow in the rat using laser-Doppler flowmetry. Parasympathetic impulses caused a rapid atropine-sensitive vasodilation followed by a maintained increase in blood flow, a portion of which remained in the presence of both atropine and L-NAME. In contrast, continuous sympathetic stimulation caused an intense vasoconstriction that was followed by a prolonged after-vasodilation. The same number of impulses delivered in bursts resulted in a cyclic vasoconstriction followed by a rapid vasodilation. Alpha-adrenoceptor blockade largely abolished the vasoconstriction, and the duration and magnitude of the after-vasodilation were reduced. Inhibition of nitric oxide (NO) synthase by L-NAME reduced the vasodilation. The addition of a beta-adrenoceptor antagonist eliminated the sympathetic vasodilator response, but in the presence of complete alpha- and beta-adrenoceptor blockade and L-NAME a small vasoconstriction remained. We conclude that the vasoconstrictor effects of sympathetic stimulation of the rat submandibular gland are due to alpha-adrenergic receptor activation and probably also NPY, and the vasodilator effects are due to NO and beta-adrenergic activity. Parasympathetic vasodilation was due to NO-independent mechanisms mediated by acetylcholine and substance P, and NO-dependent mechanisms mediated by VIP.