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

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.

1980 ◽  
Vol 239 (5) ◽  
pp. R489-R496
Author(s):  
H. T. Hammel ◽  
C. Simon-Oppermann ◽  
E. Simon

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.


1984 ◽  
Vol 247 (6) ◽  
pp. R1022-R1028
Author(s):  
R. Gerstberger ◽  
E. Simon ◽  
D. A. Gray

Saltwater-adapted ducks with functioning supraorbital salt glands were chronically implanted with a device for perfusion of the third cerebral ventricle (icv perfusion) with artificial cerebrospinal fluid (CSF) of different tonicities. The osmoregulatory responses to icv stimulation were studied at conditions of salt and water loading in which only the salt glands, both salt glands and urinary fluid excretion, or only urinary fluid excretion were stimulated; in the latter experiments plasma antidiuretic hormone (ADH) was measured with a radioimmunoassay. Hypertonic icv stimulation enhanced salt gland secretion and caused antidiuresis, due to the increase of plasma ADH. Hypotonic icv stimulation inhibited salt gland activity and caused diuresis, due to the decrease of plasma ADH. Salt gland activity, urine formation, and plasma ADH reacted more sensitively to changes of icv tonicity in the hypertonic than in the hypotonic range. The effect of icv hypotonic stimulation could be obtained also with icv perfusion of isosmotic artificial CSF deficient in NaCl content. Perfusion with artificial CSF exceeding plasma tonicity by 50 mosmol X kg-1 or more caused inhibition of salt gland secretion associated with enhanced urinary output in several experiments.


The Auk ◽  
1997 ◽  
Vol 114 (2) ◽  
pp. 242-248 ◽  
Author(s):  
Darin C. Bennett ◽  
Maryanne R. Hughes ◽  
David A. Gray

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.


1995 ◽  
Vol 73 (12) ◽  
pp. 1727-1732 ◽  
Author(s):  
Maryanne R. Hughes

Glomerular filtration rate was measured in Glaucous-winged Gulls, Larus glaucescens, acclimated to freshwater or saline and was also measured (along with salt gland secretion) following intravenous and intragastric infusion of 700 mM sodium chloride (NaCl). Freshwater- and saline-acclimated gulls had the same mean glomerular filtration rate, 5.6 ± 0.8 and 6.1 ± 1.0 mL ∙ min−1 ∙ kg−1; urine flow rate, 44 ± 20 and 46 ± 19 μL ∙ min−1 ∙ kg−1; urine/plasma osmolality ratio, 1.2 ± 0.2 and 1.7 ± 0.1; urine/plasma [14C]polyethylene glycol ratio, 210 ± 69 and 211 ± 64; and Na+ reabsorption, 99.6 ± 0.2 and 99.6 ± 0.3%, respectively. Renal function during 143 mM NaCl infusion (glomerular filtration rate, 3.4 ± 0.3 mL ∙ min−1 ∙ kg−1; urine flow rate, 19.7 ± 2.8 μL ∙ min−1 ∙ kg−1; urine/plasma osmolality ratio, 1.7 ± 0.1; urine/plasma [14C]polyethylene glycol ratio, 223 ± 26, and Na+ reabsorption 99.9 ± 0.0%) was not affected by subsequent infusion of 700 mM NaCl, although plasma osmolality was significantly increased. The urine/plasma ratio for [14C]polyethylene glycol, but not osmolality, was higher in gulls than in other avian species. Intravenously infused NaCl elicited less concentrated salt gland secretion at a significantly lower threshold plasma osmolality than intragastric NaCl infusion. Salt gland secretion and glomerular filtration rates were inversely related.Key words: bird, gull, Larus glaucescens, kidneys, salt glands, gut, sodium chloride, glomerular filtration rate, saline acclimation.


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.


1991 ◽  
Vol 261 (1) ◽  
pp. R231-R238
Author(s):  
E. Simon ◽  
D. A. Gray

Domestic ducks adapted to saline of 400 mosmol/kgH2O as their only water supply received intravenous loads of 100 mM KCl for 2 h while being intravenously infused with 200 mM NaCl at 1.0 ml/min to produce simultaneous salt gland secretion and diuresis-natriuresis. K+ loading did not alter the plasma levels of the osmoregulatory hormones arginine vasotocin, angiotensin II, aldosterone, and atrial natriuretic factor but promptly evoked kaliuresis because of a rise from 17 to 155 mM in urinary K+, with a proportional decrease in urinary Na+. Continuous infusion of amiloride (0.04 mg.min.-1.kg body wt-1 iv) further enhanced diuresis and natriuresis and lowered urinary K+, but the kaliuretic response to K+ loading was only moderately reduced because of enhanced diuresis and a rise in urinary K+ from 3 to 33 mM, with a slight decrease in urinary Na+. Changes in plasma hormone levels reflected dehydration due to excessive diuresis but were not related to kaliuresis. Salt gland secretion was not affected directly by amiloride but was secondarily reduced by the induced dehydration. In amiloride-treated ducks, hyperkalemia in response to K+ loading was exaggerated relative to the modest reduction in K+ excretion and may be attributed to moderate metabolic acidosis and/or general effects of amiloride on K+ metabolism. It is concluded that none of the established osmoregulatory hormones is involved in short-term control of renal K+ handling in ducks and that distal tubular K+ excretion involving amiloride-sensitive Na+ channels is quantitatively unimportant in this avian species.


1988 ◽  
Vol 255 (4) ◽  
pp. R575-R582 ◽  
Author(s):  
R. Gerstberger ◽  
H. Sann ◽  
E. Simon

The neuromodulatory role of vasoactive intestinal peptide (VIP) in avian salt gland secretion and blood flow was investigated in conscious saltwater-acclimated Pekin ducks. Glandular blood flow was measured by laser-Doppler flowmetry or the radioactive microspheres technique. Osmolal excretion was closely related to salt gland blood flow during salt loading. At threshold conditions of salt gland secretion, VIP infused intracarotidally induced both osmolal excretion and arteriolar vasodilation dose dependently (30-240 pmol.min-1.kg body wt-1). The VIPergic effect on the secretory process for NaCl was enhanced by simultaneous intracarotid application of acetylcholine (5 nmol.min-1.kg body wt-1), whereas the intrinsic vasodilatory potency of acetylcholine appeared to be nonadditive in coinfusion experiments. Ongoing secretion induced by systemic infusion of hypertonic saline could be suppressed by muscarinic antagonists, with salt gland blood flow being sustained at the reduced level of atropine-resistant vasodilation. Subsequent intracarotid infusion of VIP stimulated glandular blood perfusion and also, to a minor extent, osmolal excretion, suggesting an independent, functional VIP system in efferent salt gland control.


Sign in / Sign up

Export Citation Format

Share Document