Melatonin receptors and melatonin inhibition of duck salt gland secretion

Abstract

Most of the NaCl ingested by marine birds is reabsorbed from renal filtrate and excreted by the cephalic salt glands as a hypertonic NaCl secretion (SGS). Ducks have salt glands and their kidney cells have melatonin receptors. Melatonin affects glomerular filtration rate and tubular uptake of sodium (Na+) in mammals. We hypothesized that (1) duck salt glands also have melatonin receptors and (2) melatonin affects extrarenal Na+ secretion. Both hypotheses were accepted because putative melatonin receptors were identified by 2[125I]iodomelatonin binding in salt glands of Pekin ducks, Anas platyrhynchos, and because melatonin inhibited SGS in these ducks. Saline ingestion increased B(max), but not K(d), of salt gland receptors. The duration of NaCl infusion needed to stimulate SGS was positively related with preinfusion plasma melatonin concentration ([mel](pl)). Raising [mel](pl) prior to NaCl infusion further delayed onset of secretion and decreased secretion rate and concentration without affecting plasma volume and Na+ concentration. Abrupt increase in [mel](pl) during SGS immediately decreased the rate by 43%. Secretion rate remained lower than the control rate during the subsequent hour; secretion concentration was not affected. This is the first report of putative melatonin binding sites in avian salt glands. Melatonin slowed the onset of NaCl-induced salt gland secretion and decreased its rate.