Mecamylamine blocks the [Asp1,Val5]-ANG II-induced attenuation of salt gland activity in Pekin ducks.

An intravenous injection of 2 microg of [Asp1,Val5]-ANG II attenuated fluid secretion by the nasal salt glands of Pekin ducks. Ganglionic blockade with mecamylamine stopped salt gland secretion. Flow was reestablished by intravenous methacholine bromide during ganglionic blockade. A second injection of 2 microg of [Asp1, Val5]-ANG II failed to attenuate secretion during ganglionic blockade, showing that the peptide acts via the central nervous system and postganglionic parasympathetic nerves that supply the salt glands. Sympathetic nerves are located in the walls of blood vessels within the salt glands, and adrenergic fibers with "varicosities" supply extensively the secretory tubules. [Asp1, Val5]-ANG II decreased salt gland secretion both before and after alpha1-adrenergic blockade with prazosin, showing that the lowered activity was not caused by the release of norepinephrine from nerve endings and/or duck adrenal chromaffin cells. beta-Adrenergic blockade with propranolol also failed to prevent the attenuation of secretion in response to an intravenous injection of 2 microg of [Asp1,Val5]-ANG II, which showed that epinephrine did not mediate the response to the peptide.