Abstract

Nasal gland secretion was established in sea gulls by continuous infusion of hypertonic sodium chloride. Composition of nasal fluid was pH 7.08, CO₂ 10.9 mmol/l, Na⁺ 748 mmol/l, K⁺ 46 mmol/l, and Cl^- 769 mmol/l. After drug treatment or during physiological alterations the composition was unchanged, except for CO₂ and pH differences during acid-base alterations. The volumes were proportional to the excretion rates of the measured fixed ions.

Sodium bicarbonate, "tris buffer," and moderate respiratory alkalosis had no effect on nasal fluid flow. Metabolic and respiratory acidosis reduced secretion.

Carbonic anhydrase was found in the gland and in the blood. Inhibition by methazolamide reduces the volume of secretion, or abolishes it. This effect is "blocked" by severe metabolic alkalosis. The metabolic and inhibition data suggest that a requisite for secretion is an alkaline milieu within the gland.

Meralluride and aminophylline, but not chlorothiazide or hydrochlorothiazide, also reduce or abolish secretion of the nasal gland. It is suggested that mercurials and xanthines may act at the actual transport step(s), perhaps involving the same machinery as in the kidney.