Endocrine control of the nasal salt glands in birds

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Abstract
In birds, adrenocortical hormones probably sustain nasal salt gland (NSG) function, indirectly, through their influence on renal and cardiovascular function. Adrenalectomy blocks the response by duck NSG to hypertonic saline only if the ducks are maintained on freshwater. However, if adrenalectomized ducks are fed 0.9% NaCl ad libitum the NSG secrete fluid and osmolytes at the normal rate. Adrenalectomy did not prevent the significant functional hypertrophy of the NSG that always follows adaptation to saline. Mean arterial blood pressure was lower than normal two days after adrenalectomy. Stroke volume decreased by about 50% but there was a commensurate increase in cardiac frequency, so cardiac output was unchanged. There was no measurable change in total peripheral vascular resistance. There was at least a twentyfold increase in blood flow rate to the NSG when they were actively secreting fluid, but this increase was totally blocked after adrenalectomy. An inadequate supply of blood and not a corticosteriod deficiency in the secretory cells was the primary reason for NSG failure. Single intravenous injections of as little as 28 pm/kg bw of (Asp1, Val5)‐angiotensin II (AII) had no measurable effect on mean arterial blood pressure in conscious ducks but did shut off the NSG for about 4 min; then the NSG switched on again. NSG blood flow decreased after AII.

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