Role of endogenous nitric oxide in the control salivary secretion and blood flow

ABSTRACT

The present study was designed to investigate whether endogenous nitric oxide (EDNO) is involved in submandibular vasodilation and salivation induced by parasympathetic nerve stimulation. Effects of Nw-nitro-L-arginine-methyl ester (L-NAME) which blocks the synthesis of EDNO from L-arginine on the submandibular vasodilation and salivation induced by chorda stimulation or administration of various vasodilators were examined in anesthetized cats. Effect of L-NAME on K+ efflux induced by carbachol was also examined using the excised submandibular slice in vitro. In the submandibular slices, acetylcholine (10(-5) mol/L) or vasoactive intestinal polypeptide (VIP, 10(-5) mol/L) increased NO2 contents, which was prevented by pretreatment with L-NAME. Salivary secretion in response to the chorda stimulation (3 V, 1 msec, 10 ~ 20 Hz) was completely blocked by treatment with atropine (1 mg/kg). Increased blood flow response to the low frequency (1, 2, 5 Hz) stimulation was significantly reduced, whereas the blood flow induced by the higher frequency (10, 20 Hz) stimulation was not affected. Lingual-arterial infusion of L-NAME (100 mg/kg) significantly diminished the vasodilatory and salivary responses to the chorda stimulation at all stimuli frequencies used. Intra-arterial infusion of L-NAME (100 mg/kg) markedly diminished the vasodilatory responses to acetylcholine (5 mug/kg), VIP (5 mug/kg) or bradykinin (5 mug/kg). In the excised submandibular slice, K+ efflux in response to carbachol (10(-5) mol/L) was significantly decrease by pretreatment with L-NAME (10(-5) mol/L). In the isolated submandibular artery precontracted with phenylephrine (10(-5) mol/L), the vasorelaxation induced by ACh (10-7 mol/L) was reversed into a contraction by methylene blue (10(-4) mol/L). These results suggest that EDNO may play an important role in vasodilation and secretion of the submandibular gland.