Atrial Natriuretic Factor Controls Salt Gland Secretion in the Pekin Duck (Anas platyrhynchos) through Interaction with High Affinity Receptors

Endocrinology ◽  
1990 ◽  
Vol 127 (4) ◽  
pp. 1718-1726 ◽  
Author(s):  
HELMUTH SCHUTZ ◽  
RUDIGER GERSTBERGER
1997 ◽  
Vol 273 (3) ◽  
pp. R1080-R1085 ◽  
Author(s):  
D. A. Gray ◽  
C. Downing ◽  
N. Sayed

Polyclonal antibodies raised in a rabbit against avian atrial natriuretic peptide (ANP) were used to investigate the role of endogenous plasma ANP in the control of salt gland function of conscious, saltwater-adapted Pekin ducks. Salt gland secretion was initiated and maintained either by a hypervolemic (290 mosmol/kg NaCl i.v. at 2 ml/min) or hyperosmotic (1,000 mosmol/kg NaCl i.v. at 0.4 ml/min) stimulus. Both experimental conditions caused significant elevations in endogenous plasma ANP concentrations. At steady states of secretion driven by hypervolemia, the administration of ANP antiserum (anti-ANP), which reduced plasma ANP concentrations by 90%, caused an immediate 30% reduction in fluid secretion rate and sodium excretion that lasted for 20-30 min. The activity of salt glands driven by hyperosmolality was not changed by anti-ANP. The results show that the high circulating concentrations of endogenous ANP associated with conditions of sustained volume expansion promote salt gland secretion.


1989 ◽  
Vol 67 (1) ◽  
pp. 194-197 ◽  
Author(s):  
Maryanne R. Hughes

The effect of intraperitoneal NaCl loading on extracellular fluid volume, plasma concentration, and initiation of salt gland secretion was measured in freshwater- and sea water-acclimated Glaucous-winged Gulls, Larus glaucescens, and Mallards, Anas platyrhynchos. In both species salt loading was associated with a significant increase in plasma [Na] and [Cl]. In freshwater- and sea water-acclimated gulls the extracellular fluid volume increased and salt gland secretion occurred; in freshwater- and seawater-acclimated ducks the extracellular fluid volume decreased and salt gland secretion did not occur.


1969 ◽  
Vol 47 (6) ◽  
pp. 1133-1138 ◽  
Author(s):  
Maryanne Robinson Hughes ◽  
Frank E. Ruch Jr.

The spontaneously produced salt gland secretion (SGS) and tears of the domestic duck, Anas platyrhynchos, were analyzed for sodium (Na), potassium (K), and chloride (Cl) (Cl in SGS only). Acclimation to seawater did not enhance the concentrating ability of the salt glands. The NaCl concentration exceeded that of seawater by only a small margin. The tears of saline-acclimated birds contained less Na and more K than birds drinking water with low NaCl content. Salt stress significantly increased the weight of the salt glands and of the Harderian glands; the lacrymal glands were not affected. An estimation of the relative possible contribution of the cloacal fluid, SGS, and tears to cation excretion was made.


1988 ◽  
Vol 255 (3) ◽  
pp. F434-F437 ◽  
Author(s):  
F. Y. Liu ◽  
M. G. Cogan

Atrial natriuretic factor (ANF) can functionally overcome the effects of angiotensin II in several tissues. Since ANF and angiotensin II in physiological concentrations have opposite effects on renal sodium excretion, we evaluated whether functional antagonism of the two hormones occurs in the proximal convoluted tubule, as has been recently reported with use of the shrinking split-droplet technique. We used the more conventional technique of in vivo microperfusion to measure the response to systemic ANF (0.5 micrograms.kg-1.min-1) when the endogenous angiotensin II level and proximal transport were normal or when transport was first stimulated by systemic angiotensin II administration (20 ng.kg-1.min-1). In both cases, ANF did not significantly alter bicarbonate, chloride, or water transport in either the early or late proximal convoluted tubule. This inability by ANF to directly affect proximal transport is consonant with the known lack of high-affinity receptors and appropriate second messenger system for ANF in the proximal convoluted tubule.


1983 ◽  
Vol 149 (4) ◽  
pp. 451-456 ◽  
Author(s):  
H. T. Hammel ◽  
C. Simon-Oppermann ◽  
E. Simon

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