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Am J Physiol Heart Circ Physiol (July 11, 2002). doi:10.1152/ajpheart.01071.2001
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Articles in PresS, published online ahead of print July 11, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01071.2001
Submitted on December 6, 2001
Accepted on July 10, 2002

The extracellular signal-regulated kinase pathway regulates Na+-HCO3- cotransport activity in adult rat cardiomyocytes

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

1 Universite Paris XI, Laboratoire de Physiologie Cellulaire, CNRS ESA 8078, Hopital Marie Lannelongue, Orsay, 91405, France
2 King's College London, The Rayne Institute, St Thomas' Hospital, Centre for Cardiovascular Biology and Medicine, London, SE1 7EH, United Kingdom

* To whom correspondence should be addressed. E-mail: danielle.feuvray{at}ibaic.u-psud.fr.

The sarcolemmal Na+-HCO3- cotransporter (NBC) is stimulated by intracellular acidification and acts as an acid extruder. We examined the role of the extracellular signal-regulated kinase (ERK) pathway of the mitogen-activated protein kinase (MAPK) cascade as a potential mediator of NBC activation by intracellular acidification in the presence and absence of angiotensin II, in adult rat ventricular myocytes. Intracellular pH (pHi) was recorded using seminaphthorhodafluor-1. The NH4+ method was used to induce an intracellular acid load. NBC activation was significantly decreased by the two ERK inhibitors PD98059 and U0126. NBC activity after acidification was increased in the presence of Ang II (pHi range 6.75-7.00). Ang II plus PD123319 (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 U0126. 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 angiotensin II.




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