The effect of carbonic anhydrase inhibitors on secretion by the parotid and mandibular glands of red kangaroos Macropus rufus.
The effects of carbonic anhydrase inhibitors on secretion by macropodine parotid and mandibular glands were investigated using anaesthetized red kangaroos. In the parotid gland, acetazolamide (500 mumol.l-1) reduced a stable acetylcholine-evoked, half-maximal flow rate of 2.02 +/- 0.034 to 0.27 +/- 0.023 ml.min-1 (87% reduction). Concurrently, salivary bicarbonate concentration and secretion fell (129.4 +/- 1.46 to 80.9 +/- 1.63 mmol.l-1 and 264.8 +/- 7.96 to 22.3 +/- 2.30 mumol.min-1, respectively), phosphate and chloride concentrations rose (14.0 +/- 0.79 to 27.6 +/- 0.85 mmol.l-1 and 5.6 +/- 0.25 to 27.5 +/- 1.32 mmol.l-1, respectively), sodium concentration and osmolality were unaltered, and potassium concentration fell (8.8 +/- 0.33 to 6.4 +/- 0.29 mmol.l-1). High-rate cholinergic stimulation during acetazolamide blockade was unable to increase salivary flow beyond 11 +/- 0.9% of that for equivalent unblocked control stimulation. However, superimposition of isoprenaline infusion on the acetylcholine stimulation caused a three-fold increase in the blocked flow rate. These treatments were accompanied by small increases in salivary phosphate and chloride concentrations but not bicarbonate concentration. Methazolamide infusion caused similar changes in parotid secretion. In the mandibular gland, acetazolamide infusion had no effect on salivary flow rate during either low- or high-level acetylcholine stimulation. Acetazolamide caused no alterations in salivary electrolyte secretion at low flow rates, but curtailed the rise in bicarbonate concentration associated with high-level acetylcholine stimulation. Acetazolamide administration did not affect the increase in salivary flow rate associated with isoprenaline infusion, but did block the concomitant increase in bicarbonate concentration and secretion substantially.(ABSTRACT TRUNCATED AT 250 WORDS)
Beal
A M
AM
School of Biological Science, University of New South Wales, Kensington, Australia.
D000109:Acetylcholine / Q000494:pharmacology; D000320:Adrenergic Fibers / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology*; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D002799:Cholinergic Fibers / Q000187:drug effects / Q000502:physiology; D005260:Female; D007545:Isoproterenol / Q000494:pharmacology; D007614:Macropodidae / Q000378:metabolism* / Q000502:physiology; D008297:Male; D008704:Methazolamide / Q000494:pharmacology; D009994:Osmolar Concentration; D010306:Parotid Gland / Q000378:metabolism* / Q000502:physiology; D010710:Phosphates / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D012469:Salivary Glands / Q000378:metabolism* / Q000502:physiology; D012964:Sodium / Q000378:metabolism
D001639:Bicarbonates; D002257:Carbonic Anhydrase Inhibitors; D002712:Chlorides; D010710:Phosphates; D012964:Sodium; D007545:Isoproterenol; D000109:Acetylcholine; D011188:Potassium; D008704:Methazolamide