Metabolic acidosis,prostaglandin E2 and insulin stimulates intracellular free calcium ([Ca2+]1) in isolated cells of toad urinary bladder |
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| Institution: | 1. Department of Biomedical Sciences, Baylor College of Dentistry, Dallas, TX 75246, U.S.A.;1. Department of Physiology and Biophysics, The State University of New York, The University at Buffalo, Buffalo, NY 14203, USA;2. Department of Ophthalmology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA;3. State University of New York Eye Institute, University at Buffalo, The State University of New York, Buffalo, NY, USA;4. Department of Physiology and Biophysics, Case Western Reserve University, School of Medicine, Cleveland, OH 44106, USA |
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| Abstract: | 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. Protaglandin E2 (PGE2) (10−5M) 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+. |
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