Abstract
It is well known that metabolic acidosis (MA), PGE 2, and insulin stimulate H + excretion in toad urinary bladder. In addition, PGE 2 has been shown to increase in the toad bladder during MA. Our present experimental findings indicate that MA, PGE 2 and insulin increase [Ca 2+] 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 Ca 2+ ([Ca 2+] i) than similar cells obtained from toads in normal acid-base balance. Protaglandin E 2 (PGE 2) (10 −5M) was found to stimulate [Ca 2+] 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 [Ca 2+] i, in toad bladder cells ( P < 0.01). The increase in [Ca 2+] i following PGE 2 stimulation was not dependent on extracellular Ca 2+, whereas the increase seen following insulin stimulation was dependent on extracellular Ca 2+.
Published Version
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