NEURAL REGULATION OF BLOOD-FLOW IN THE RAT SUBMANDIBULAR-GLAND

Blood flow in salivary glands is regulated mainly by sympathetic and p arasympathetic 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 r at using laser-Doppler flowmetry. Parasympathetic impulses caused a ra pid atropine-sensitive vasodilation followed by a maintained increase in blood flow, a portion of which remained in the presence of both atr opine and L-NAME. In contrast, continuous sympathetic stimulation caus ed 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. Inhibit ion of nitric oxide (NO) synthase by L-NAME reduced the vasodilation. The addition of a beta-adrenoceptor antagonist eliminated the sympathe tic vasodilator response, but in the presence of complete alpha- and b eta-adrenoceptor blockade and L-NAME a small vasoconstriction remained . We conclude that the vasoconstrictor effects of sympathetic stimulat ion of the rat submandibular,oland are due to alpha-adrenergic recepto r activation and probably also NPY, and the vasodilator effects are du e to NO and beta-adrenergic activity. Parasympathetic vasodilation was due to NO-independent mechanisms mediated by acetylcholine and substa nce P, and NO-dependent mechanisms mediated by VIP.