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Department of Zoology, University of Toronto, Toronto, Ontario, M5S 3G5, Canada
An intravenous injection of 2 µg 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 µg 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
1-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.
-Adrenergic blockade with propranolol also failed
to prevent the attenuation of secretion in response to an intravenous
injection of 2 µg of [Asp1,Val5]-ANG
II, which showed that epinephrine did not mediate the response to the peptide.
ganglionic blockade; acetylcholine; catecholamines
This article has been cited by other articles:
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M. K. Heinz and D. A. Gray Role of plasma ANG II in the excretion of acute sodium load in a bird with salt glands (Anas platyrhynchos) Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2001; 281(1): R346 - R351. [Abstract] [Full Text] [PDF] |
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