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

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.

Endogenous plasma atrial natriuretic peptide and the control of salt gland function in the Pekin duck

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.

Responses of gull kidneys and salt glands to NaCl loading

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.

Control of renal handling of potassium loads in ducks with active salt glands

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.

Extracellular fluid volume and the initiation of salt gland secretion in ducks and gulls

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.