Angiotensin II-activated Ca2+ entry-induced release of Ca2+ from intracellular stores in rat portal vein myocytes. |
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Authors: | J. L. Morel, N. Macrez-Leprê tre, J. Mironneau |
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Affiliation: | J. L. Morel, N. Macrez-Leprêtre, and J. Mironneau |
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Abstract: | 1. The action of angiotensin II (AII) was studied in single myocytes from rat portal vein in which the cytoplasmic Ca2+ concentration was estimated by emission from dyes Fura-2 or Indo-1 and the Ca2+ channel current was measured with the whole-cell mode of the patch-clamp technique. 2. Most of the AII-evoked increases in [Ca2+]i were reduced by about 60% after pretreatment with ryanodine and caffeine to deplete intracellular Ca2+ stores. However, in some cells the AII-induced Ca2+ responses were of small amplitude and resembled those obtained in the presence of ryanodine and caffeine. Both types of Ca2+ responses induced by AII were selectively inhibited by losartan, suggesting that the AII effects resulted from activation of the angiotensin AT1 receptors. 3. The concentration-response curve to AII had an EC50 value close to 1 nM for the increase in [Ca2+]i obtained after depletion of intracellular Ca2+ stores. This value was increased to around 18 nM in experiments where the intracellular Ca2+ stores were not depleted. 4. AII-evoked Ca2+ responses were abolished in the absence of external Ca2+ and in the presence of 1 microM oxodipine to block L-type Ca2+ channels. 5. Intracellular applications of the InsP3 receptor antagonist, heparin or an anti-PdtIns antibody did not modify AII-induced Ca2+ responses. 6. Our results show that AII releases Ca2+ from intracellular stores without involving InsP3 but through a Ca2+ release mechanism activated by Ca2+ influx through L-type Ca2+ channels. |
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