α1-Adrenoceptor and purinoceptor agonists modulate Na-H antiport in single cardiac cells

M. Puceat, O. Clement-Chomienne, Andre Terzic, G. Vassort

Research output: Contribution to journalArticle

60 Citations (Scopus)

Abstract

We investigated the effects of an α1-adrenoceptor (phenylephrine) and a purinoceptor agonist (ATP), both of which accelerate the phosphoinositide turnover, on the Na-H antiport activity of rat single cardiac cells using the pH-sensitive fluorescent indicator seminaphthorhodafluor-1 (SNARF-1). Both phenylephrine, in the presence of a β-adrenoceptor blocker, and ATP enhanced the ability of the cell to regulate its intracellular pH (pH(i)) after an imposed acid load. This effect was observed in HCO3-free N-2- hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) and prevented by Na- H antiport inhibitors ethylisopropylamiloride (EIPA) or amiloride. Similar results were obtained when cells were bathed in an acidic extracellular medium. Hence, the α1-adrenoceptor and purinoceptor agonists activate the Na-H antiport even when it is partially inhibited by extracellular protons. To further evaluate the effects of the two neurohormones, the rate of proton efflux was estimated as a function of the magnitude of the imposed acid load. The results indicate that the agonist-induced modulation of the Na-H antiport is caused by an acceleration of its exchange activity and by a shift of its dependence on pH(i) toward more alkaline pH values. The agonist-mediated stimulation of the antiport was also observed in partially depolarized cells and was not dependent on intracellular Ca. Phorbol 12-myristate 13-acetate was not able to reproduce the effects of the agonists on the Na-H antiport. Conversely, the inhibitors of protein kinase C did not prevent the activation of the antiport by the neurohormones. Thus our data suggest that neither a Ca-calmodulin-dependent kinase nor protein kinase C is responsible for the α1-adrenoceptor- and purinoceptor-mediated stimulation of the antiport.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume264
Issue number2 33-2
StatePublished - 1993
Externally publishedYes

Fingerprint

Purinergic Agonists
Ion Transport
Adrenergic Receptors
Phenylephrine
Protein Kinase C
Neurotransmitter Agents
Protons
Adenosine Triphosphate
HEPES
Purinergic Receptors
Calcium-Calmodulin-Dependent Protein Kinases
Acids
Amiloride
Phosphatidylinositols
Acetates

Keywords

  • intracellular pH
  • protein kinase C
  • sodium-hydrogen antiport

ASJC Scopus subject areas

  • Physiology

Cite this

α1-Adrenoceptor and purinoceptor agonists modulate Na-H antiport in single cardiac cells. / Puceat, M.; Clement-Chomienne, O.; Terzic, Andre; Vassort, G.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 264, No. 2 33-2, 1993.

Research output: Contribution to journalArticle

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