The role of nitric oxide in the control of protein secretion in the parotid gland of anaesthetized sheep.

Abstract

Parotid secretion has been investigated in anaesthetized lambs in the presence and absence of N omega-nitro-L-arginine methyl ester (L-NAME) and sodium nitroprusside to block de novo synthesis of nitric oxide (NO). Following administration of L-NAME the basal rate of flow was unaffected and changes in electrolyte secretion failed to achieve statistical significance but there was a significant fall in the basal rate of protein secretion. The flow of parotid saliva which occurred in response to stimulation of the parasympathetic innervation was reduced by 34% and sodium output was reduced in approximately the same proportion. L-NAME had no significant effect on these parameters during stimulation of the sympathetic innervation. During combined stimulation of the parasympathetic and sympathetic innervations L-NAME caused a reduction in parotid salivary flow and sodium output which was roughly the same as that observed during parasympathetic stimulation alone. However, L-NAME caused a much greater reduction in protein output during each of these experimental protocols: -92% during parasympathetic stimulation, =63% during sympathetic stimulation, and -60% during combined stimulation. Whereas the absolute amount of protein secreted was reduced after L-NAME in each instance, the extent of potentiation of protein output recorded during combined stimulation was increased roughly fivefold. It is concluded that the output of protein in response to autonomic stimulation exhibits a greater No dependence than either the flow of saliva or secretion of electrolytes in this gland.