Angiotensin II-activated Ca2+ entry-induced release of Ca2+ from intracellular stores in rat portal vein myocytes

J.L. Morel, N. Macrez-Leprêtre, J. Mironneau
British Journal of Pharmacology. 1996-05-01; 118(1): 73-78
DOI: 10.1111/j.1476-5381.1996.tb15368.x

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1. Br J Pharmacol. 1996 May;118(1):73-8.

Angiotensin II-activated Ca2+ entry-induced release of Ca2+ from intracellular
stores in rat portal vein myocytes.

Morel JL(1), Macrez-Leprêtre N, Mironneau J.

Author information:
(1)Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, URA CNRS
1489, Université de Bordeaux II, France.

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.

DOI: 10.1111/j.1476-5381.1996.tb15368.x
PMCID: PMC1909499
PMID: 8733578 [Indexed for MEDLINE]

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