title: The effect of transport-blocking drugs on secretion of fluid and electrolytes by the mandibular gland of red kangaroos, Macropus rufus.
abstract: Mechanisms of primary fluid formation by macropodine mandibular glands were investigated in anaesthetized red kangaroos using ion-transport and carbonic anhydrase inhibitors. Bumetanide at carotid plasma concentrations of 0.005-0.1 mmol/l progressively reduced a stable, acetylcholine-evoked flow rate of 1.02 +/- 0.024 ml/min to 0.16 +/- 0.016 ml/min (mean +/- SEM). Concurrently, saliva [Na], [Cl] and osmolality decreased, [K] and [HCO3] increased and HCO3 excretion was unaffected. High-rate cholinergic stimulation was unable to increase salivary flow above 12 +/- 1.5% of that for equivalent pre-bumetanide stimulation. Furosemide (1.0 mmol/l) and ethacrynate (0.5 mmol/l) caused depression of salivary flow and qualitatively similar effects on ion concentrations to those of bumetanide. Amiloride (up to 0.5 mmol/l) caused no reduction in salivary flow rates or [Na] but decreased [K] and [Cl] and increased [HCO3]. When compared with bumetanide alone, amiloride combined with bumetanide further augmented [K] and [HCO3] and lowered [Cl], but had no additional effects on Na or flow. At the higher level, 4-acetamido-4'- isothiocyanatostilbene-2,2'disulphonic acid (SITS) (0.05 and 0.5 mmol/l) stimulated fluid output, increased [HCO3] and [protein], and depressed [Na], [K] and [Cl]. Relative to bumetanide alone, SITS given with bumetanide had no additional effects on salivary flow or electrolytes. Methazolamide (0.5 mmol/l) in combination with bumetanide curtailed the decrease in [Cl] and the increases in [K] and [HCO3] associated with bumetanide. The residual methazolamide-resistant HCO3 excretion was sufficient to support 2-6% of primary fluid secretion. It was concluded that secretion of primary fluid by the kangaroo mandibular gland is initiated mainly (> 90%) by Cl transport resulting from Na-K-2Cl symport activity. A small proportion of the fluid secretion (up to 6%) appears to be supported by HCO3 secretion. No evidence was found for fluid secretion being dependent on Cl transport involving Na/H and Cl/HCO3 antiports or on HCO3 synthesis involving carbonic anhydrase.
authors.affiliation: School of Biological Science, University of New South Wales, Sydney, Australia.
authors.forename: A M
authors.initials: AM
authors.lastname: Beal
mesh_terms: D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000494:pharmacology; D000109:Acetylcholine / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002034:Bumetanide / Q000097:blood / Q000494:pharmacology; D002254:Carbonates / Q000032:analysis; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology; D002713:Chlorine / Q000032:analysis; D018678:Cholinergic Agents / Q000494:pharmacology; D004232:Diuretics / Q000097:blood / Q000494:pharmacology; D004573:Electrolytes / Q000032:analysis*; D004976:Ethacrynic Acid / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D017136:Ion Transport / Q000187:drug effects; D007614:Macropodidae; D008704:Methazolamide / Q000494:pharmacology; D009994:Osmolar Concentration; D011188:Potassium / Q000032:analysis; D012463:Saliva / Q000737:chemistry / Q000187:drug effects* / Q000378:metabolism; D012469:Salivary Glands / Q000187:drug effects* / Q000378:metabolism; D012471:Salivary Proteins and Peptides / Q000032:analysis / Q000187:drug effects / Q000378:metabolism; D012636:Secretory Rate / Q000187:drug effects; D012964:Sodium / Q000032:analysis
chemical_list: D002254:Carbonates; D002257:Carbonic Anhydrase Inhibitors; D018678:Cholinergic Agents; D004232:Diuretics; D004573:Electrolytes; D012471:Salivary Proteins and Peptides; D002034:Bumetanide; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D002713:Chlorine; D000584:Amiloride; D005665:Furosemide; D012964:Sodium; D004976:Ethacrynic Acid; D000109:Acetylcholine; D011188:Potassium; D008704:Methazolamide