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Actions of the phorbol ester, PMA, on ATP‐induced fluctuations in cytoplasmic calcium in single isolated bovine aortic endothelial cells
Author(s) -
Lynch M,
Gillespie JI,
Johnson C
Publication year - 1992
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1992.sp003631
Subject(s) - forskolin , adenylate kinase , phorbol , diacylglycerol kinase , protein kinase c , intracellular , biophysics , cyclase , medicine , endocrinology , biology , chemistry , microbiology and biotechnology , stimulation , biochemistry , enzyme
Agonist‐evoked rises in [Ca2+]i were recorded from single bovine aortic endothelial cells in the middle of confluent monolayers by dual‐wavelength microspectrofluorimetry. Low doses of ATP (1‐5 microM) induced a transient rise in [Ca2+]i followed by a maintained plateau phase upon which were superimposed irregular fluctuations in [Ca2+]i. The mechanism underlying these fluctuations is not known. Addition of the phorbol ester, phorbol 12‐myristate 13‐acetate (PMA), to single cells displaying ATP‐induced fluctuations reduced the amplitude and frequency of these fluctuations but the maintained plateau phase was unaffected. Elevation of intracellular cAMP by activation of adenylate cyclase with forskolin, or application of dibutyryl cAMP did not affect the ATP‐induced fluctuations. These results suggest a possible role for the diacylglycerol limb of the phosphoinositide hydrolysis pathway, via activation of protein kinase C, but not cAMP, in the mechanism responsible for generating ATP‐induced fluctuations in [Ca2+]i.