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Am J Physiol Heart Circ Physiol 283: H2102-H2109, 2002. First published July 11, 2002; doi:10.1152/ajpheart.01071.2001
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01071.2001v1
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Vol. 283, Issue 5, H2102-H2109, November 2002

The ERK pathway regulates Na+-HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> cotransport activity in adult rat cardiomyocytes

Delphine Baetz1, Robert S. Haworth2, Metin Avkiran2, and Danielle Feuvray1

1 Laboratoire de Physiologie Cellulaire and Centre National de la Recherche Scientifique, Hôpital Marie Lannelongue-Université Paris XI, 91405 Orsay Cedex, France; and 2 Centre for Cardiovascular Biology and Medicine, King's College London, The Rayne Institute, St. Thomas' Hospital, London 7E1 7EH, United Kingdom

The sarcolemmal Na+-HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> cotransporter (NBC) is stimulated by intracellular acidification and acts as an acid extruder. We examined the role of the ERK pathway of the MAPK cascade as a potential mediator of NBC activation by intracellular acidification in the presence and absence of angiotensin II (ANG II) in adult rat ventricular myocytes. Intracellular pH (pHi) was recorded with the use of seminaphthorhodafluor-1. The NH<UP><SUB>4</SUB><SUP>+</SUP></UP> method was used to induce an intracellular acid load. NBC activation was significantly decreased with the ERK inhibitors PD-98059 and U-0126. NBC activity after acidification was increased in the presence of ANG II (pHi range of 6.75-7.00). ANG II plus PD-123319 (AT2 antagonist) still increased NBC activity, whereas ANG II plus losartan (AT1 antagonist) did not affect it. ERK phosphorylation (measured by immunoblot analysis) during intracellular acidification was increased by ANG II, an effect that was abolished by losartan and U-0126. In conclusion, the MAPK(ERK)-dependent pathway facilitates the rate of pHi recovery from acid load through NBC activity and is involved in the AT1 receptor-mediated stimulation of such activity by ANG II.

cardiac ventricular myocytes; angiotensin II


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