Nitric oxide modulates salivary amylase and fluid, but not epidermal growth factor secretion in conscious rats

The involvement of the L-arginine/NO pathway in the control of salivary flu id, amylase and epidermal growth factor (EGF) secretion was investigated in conscious rats. For the collection of saliva, an oesophageal cannula was i mplanted. To obtain steady secretion, submaximal carbachol background infus ion was given. Different treatments included NO synthase inhibitor N-G-nitr o-L-arginine (NOLA; with or without phentolamine, propranolol), L-arginine, D-arginine and NO donor 3-morpholinosydnonimine (SIN-1) administration. Vo lume, amylase activity and EGF output in the secreted fluid were determined in 30 min mixed saliva samples. Carbachol infusion alone produced a modest , sustained salivary fluid and amylase secretion. NOLA (30 mg/kg) further i ncreased both fluid (p<0.001) and amylase outputs (p<0.001). These latter e ffects were prevented by L-arginine but not by D-arginine or by phentolamin e. Propranolol administration decreased both fluid and amylase secretion be low the carbachol plateau, and NOLA did not modify this suppressed secretor y rate. SIN-1 did not alter either volume or amylase secretion. Interesting ly, NOLA given without carbachol did not modify salivation. Neither carbach ol nor NOLA changed salivary EGF output. The present results suggest that t he L-arginine/NO pathway has a modulatory role in the cholinergic control o f salivary amylase secretion, but not in EGF output. The mechanisms of inhi bitory action of NO on salivary fluid and amylase secretion remain to be id entified.