Mechanism of substance P-induced salivary secretion in the rat: effect of substance P on autonomic nervous system and prostaglandin synthesis (author's transl)

Salivary flow and amylase secretion induced by substance P(SP) administered intraventricularly were considerably less than that by SP given intravenously (i.v.). Salivary flow induced by SP (i.v.) was partially inhibited by baclofen, atropine, d-tubocurarine, alcuronium, phenylephrine and PGE2, while it was enhanced by arachidonic acid and indomethacin. Salivary amylase secretion induced by SP given i.v. was enhanced markedly by isoproterenol, phenoxybenzamine, phentolamine and No. 865-123 (an adrenergic neuron blocking agent), and moderately by baclofen, PGE2 and arachidonic acid, while it was not influenced by propranolol. The enhancements of amylase secretion by adrenergic alpha-blockers were completely inhibited by propranolol. The in vitro examination using rat brain synaptosomes showed that SP promoted markedly the synthesis of PGs, especially of PGE2. These results suggest that the SP-receptor has a nicotinic receptor-like property and may be closely related to adrenergic alpha-receptors situated postsynaptically and presynaptically and to postsynaptic PGE2-receptors. From these results, it is concluded that SP-induced salivary flow and amylase secretion are modulated by the promotion of PGs synthesis in the autonomic nervous system.