MECHANISMS OF FLUID AND ION SECRETION HY THE PAROTID-GLAND OF THE KANGAROO, MACROPUS-RUFUS, ASSESSED BY ADMINISTRATION OF TRANSPORT-INHIBITING DRUGS

Possible mechanisms of primary fluid formation by macropodine parotid glands were investigated in anaesthetized red kangaroos using ion tran sport inhibitors. Carotid plasma amiloride Concentrations of 0.05-0.5 mmol . l(-1) progressively reduced a stable acetylcholine-evoked half- maximal flow rate of 2.0 +/- 0.04 to 0.22 +/- 0.024 mi min(-1) (mean /- SEM). Concurrently, saliva bicarbonate concentration and secretion fell (135 +/- 1.6 to 67 +/- 1.7 mmol . l(-1) and 272 +/- 7.6 to 15 +/- 2.6 mu mol . min(-1), respectively); [phosphate], [chloride] and [sod ium] rose and [potassium] and osmolality were unaltered. High-rate cho linergic stimulation did not increase saliva flow beyond 11 +/- 1.0% o f that for equivalent pre-amiloride stimulation. Equipotent levels of amiloride and methazolamide given concurrently were no more effective at blocking flow and bicarbonate secretion than when given separately. Furosemide (up to 2 mmol . l(-1)), bumetanide (up to 0.2 mmol . l(-1) ) and ethacrynate (1 mmol . l(-1)) in carotid plasma had no effect on salivary flow or ion concentrations. During methazolamide blockade, fu rosemide did not curtail the concurrent increase in salivary [chloride ]. Chlorothiazide at 0.25-1.0 mmol . l(-1) caused progressive depressi on of saliva flow and [bicarbonate], and elevation of [chloride]. 4-ac etamido-4'-isothiocyanatostilbene-2, phonic acid at 0.1 mmol . l(-1) w as without effect, whereas at 0.5 mmol . l(-1) it stimulated fluid sec retion and increased saliva [protein], [sodium], [potassium], [bicarbo nate] and osmolality. Concurrently, mean arterial blood pressure and p ulse pressure fell and heart rate, haematocrit and carotid artery plas ma flow rose. These responses were absent if saliva flow was kept cons tant by reduction in cholinergic stimulation during acetamido-4-isothi ocyanatostilbene-2,2'disulphonic acid administration. It is concluded that secretion of primary fluid by the kangaroo parotid is initiated m ainly (> 90%) by secretion of bicarbonate which is formed in the endpi ece cells from CO2 delivered by the circulation. No evidence was found for initiation of fluid secretion by chloride transport involving bas olateral Na+-K+-2Cl(-) symports, Na+-Cl- symports or Cl-1/HCO3- antipo rts.