Metabolic acidosis, prostaglandin E2 and insulin stimulates intracellular free calcium ([Ca2+]i) in isolated cells of toad urinary bladder.
It is well known that metabolic acidosis (MA), PGE2, and insulin stimulate H+ excretion in toad urinary bladder. In addition, PGE2 has been shown to increase in the toad bladder during MA. Our present experimental findings indicate that MA, PGE2 and insulin increase [Ca2+]i and this then may be the signal for stimulation of H+ excretion in this tissue. Isolated cells of the toad urinary bladder, obtained from toads in a chronic metabolic acidosis (MA) have a significantly higher intracellular Ca2+ ([Ca2+]i) than similar cells obtained from toads in normal acid-base balance. Prostaglandin E2 (PGE2) (10(-5) M) was found to stimulate [Ca2+]i in the same normal toad bladder cells, as determined by the fluorescence ratio technique using FURA 2/AM (P < 0.05). Insulin (100 mU/ml) was also found to stimulate [Ca2+]i in toad bladder cells (P < 0.01). The increase in [Ca2+]i following PGE2 stimulation was not dependent on extracellular Ca2+, whereas the increase seen following insulin stimulation was dependent on extracellular Ca2+.
Department of Biomedical Sciences, Baylor College of Dentistry, Dallas, TX 75246.
L W
LW
Frazier
D000138:Acidosis / Q000378:metabolism*; D000818:Animals; D002024:Bufo marinus; D002118:Calcium / Q000378:metabolism*; D015232:Dinoprostone / Q000494:pharmacology*; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology*; D001743:Urinary Bladder / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism
D007328:Insulin; D015232:Dinoprostone; D002118:Calcium