ANG II-induced attenuation of duck salt gland secretion does not depend upon the release of adrenal catecholamines

2005 ◽  
Vol 176 (1) ◽  
pp. 35-43 ◽  
Author(s):  
David Gordon Butler ◽  
Wallace Lam ◽  
Jeff Tong
Keyword(s):  
Salt Gland ◽  
Gland Secretion ◽  
Ang Ii ◽  
Salt Gland Secretion

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

1999 ◽  
Vol 277 (3) ◽  
pp. R836-R842 ◽  
Author(s):  
David Gordon Butler
Keyword(s):  
Intravenous Injection ◽  
Salt Gland ◽  
Sympathetic Nerves ◽  
Gland Secretion ◽  
Adrenergic Blockade ◽  
Ang Ii ◽  
Salt Glands ◽  
Ganglionic Blockade ◽  
Pekin Ducks ◽  
Salt Gland Secretion

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 α1-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. β-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.

Cation content of salt gland secretion and tears in the brolga, Grus rubicundus (Perry) (Aves : Gruidae)

1973 ◽  
Vol 21 (4) ◽  
pp. 515 ◽  
Author(s):  
MR Hughes ◽  
JG Blackman
Keyword(s):  
Salt Gland ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Gland Secretion ◽  
Plasma Sodium ◽  
First Report ◽  
Gland Size ◽  
Cation Content ◽  
Salt Gland Secretion ◽  
Sodium And Potassium

This is the first report of salt gland secretion in cranes (Gruidae). The sodium and potassium concentrations of the plasma, tears, salt gland secretion, and urine of the brolga were determined. Tear sodium was equal to plasma sodium; tear plasma was four times as concentrated as plasma potassium. These values were normal for tears. The salt gland secretion sodium concentration (about 300 m-equivll) was lower than that reported for other NaC1-injected birds. This may be due to the diet, small gland size, or to insufficient stress. The salt gland secretion to plasma ratios were the same for sodium and potassium. This is unusual. The urine had a lower sodium concentration than the plasma.

Effect of volume expansion and veratrine on salt gland secretion in the goose

1977 ◽  
Vol 232 (5) ◽  
pp. R185-R189
Author(s):  
I. H. Zucker ◽  
C. Gilmore ◽  
J. Dietz ◽  
J. P. Gilmore
Keyword(s):  
Volume Expansion ◽  
Plasma Osmolality ◽  
Salt Gland ◽  
Sodium Concentration ◽  
Ringer Solution ◽  
Gland Secretion ◽  
Similar Increase ◽  
Volume Load ◽  
Salt Gland Secretion ◽  
Peripheral Receptor

The influence of acute intravascular volume expansion on salt gland secretion of conscious, adult geese was investigated. The intravenous administration of 5% dextran in Krebs-bicarbonate-Ringer solution in an amount equivalent to 30% of the estimated blood volume caused a transient but highly significant increase in salt gland secretion independent of changes in plasma osmolality or sodium concentration. Intravenous veratrine (60 microng) caused a similar increase in salt gland secretion only when administered after the volume load. Intravenous 5% NaCl always caused a prolonged and significant increase in salt gland secretion which was not potentiated by veratrine. Volume expansion and hypertonic saline caused a significant tachycardia while veratrine caused a significant bradycardia. It is concluded that a volume component may contribute to the initiation of salt gland secretion in the goose and that the peripheral receptor involved is most likely vascular in origin.

CONTROL OF THE SALT-SECRETING GLAND OF THE DUCK: I. OSMOTIC REGULATION

1967 ◽  
Vol 45 (6) ◽  
pp. 925-936 ◽  
Author(s):  
André Lanthier ◽  
Thomas Sandor
Keyword(s):  
Sodium Chloride ◽  
Sodium Bicarbonate ◽  
Intravenous Infusion ◽  
Electrolyte Concentration ◽  
Salt Gland ◽  
The Other ◽  
Gland Secretion ◽  
Osmotic Regulation ◽  
Domestic Duck ◽  
Salt Gland Secretion

The osmotic regulation of the salt gland secretion was studied in the domestic duck. The response to the intravenous infusion of 5% sodium chloride (850 meq Na per liter) was established in unanesthetized ducks. Sodium bicarbonate (892 meq Na/l) produced a salt gland secretion similar to that after 5% sodium chloride, except that it was accompanied by a moderate diuresis. Mannitol and sucrose had similar effects. On the other hand, urea, ammonium chloride, dextran, and meralluride produced only a small amount of salt-gland secretion of low electrolyte concentration. Antidiuretic doses of Pitressin did not induce secretion of the salt gland.

Properties of body fluids influencing salt gland secretion in Pekin ducks

1980 ◽  
Vol 239 (5) ◽  
pp. R489-R496
Author(s):  
H. T. Hammel ◽  
C. Simon-Oppermann ◽  
E. Simon
Keyword(s):  
Extracellular Fluid ◽  
Salt Gland ◽  
Colloid Osmotic Pressure ◽  
Threshold Concentration ◽  
Gland Secretion ◽  
Salt Glands ◽  
Control Solution ◽  
Pekin Ducks ◽  
Salt Gland Secretion ◽  
Before And After

Pekin ducks were reared and maintained on 620 mosmol NaCl/kg H2O to enhance the secretory capability of their salt glands. When a control solution of 1,000 mosmol NaCl/kg H2O was infused intravenously at 0.2, 0.4, or 0.6 ml/min for 60-90 min, the infused loads were secreted in approximately equal quantities, indicating that the amount of NaCl in the extracellular fluid (ECF) before and after each infusion did not change. Salt and water secreted in response to experimental infusions of hyposmotic saline or blood were less than the solute and water infused. Thus, ECF volume increased and the Na+ concentration decreased. Infusions of control solution followed these experimental infusions. The salt and water secreted again equaled the amounts infused, indicating that the threshold concentration of Na+ ([Na+]th) for salt gland secretion was decreased by the increase in ECF volume. When the colloid dextran was added to the control solution, its infusion increased the colloid osmotic pressure of the blood and decreased nasal secretion. Because dextran increased the intravascular volume while the interstitial fluid volume (ISFV) decreased, we conclude that the [Na+]th was inversely correlated with ISFV.

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