caa a22 4500 469078596 CHVBK 20180323132942.0 cr unu---uuuuu 170328e19921101xx s 000 0 eng 10.1007/BF00169019 doi (NATIONALLICENCE)springer-10.1007/BF00169019 Phenylephrine and ATP enhance an amiloride insensitive bicarbonate-dependent alkalinizing mechanism in rat single cardiomyocytes [Elektronische Daten] [André Terzic, Michel Pucéat, Odile Clément-Chomienne, Guy Vassort] Summary: To expel the excess protons generated during a cellular acidification and to fully recover basal intracellular pH (pHi), cardiac cells rely on the amiloride-sensitive Na/H antiport. We report that rat single ventricular cardiomyocytes, loaded with the fluorescent pH indicator Snarf-1 and treated with inhibitors of the Na/H antiport, amiloride or its analogues, partially restored their pHi through a bicarbonate-dependent mechanism following an acidosis (imposed by the ammonia-pulse technique). In the presence of ethylisopropylamiloride (10 μM) or amiloride (1 mM) and 25 mM bicarbonate in the extracellular solution, the average time that cells needed to recover half of their pHi, following the removal of 20 mM NH4Cl, was 3.4 min, while the rate of proton efflux was calculated to be 2.0 mM/min. The stilbene derivative, 4-4′-di-isothiocyanostilbene-2,2′-disulphonate (DIDS 200 μM), a known blocker of anion transporters, inhibited this recovery. Both phenylephrine (100 μM, 3 μM propranolol present), an al-adrenoceptor agonist, and ATP (10 μM), a purinergic agonist, significantly enhanced the rate of proton efflux that was due to this HC03-dependent alkalinizing mechanism. Phenylephrine and ATP also shortened by three-fold the time that a myocyte needed to recover half of its initial pHi. This bicarbonate-dependent alkalinizing mechanism could provide an additional means by which cardiac cells recover their pHi from acidosis, especially under conditions in which the Na/H antiport is inhibited. Furthermore, catecholamines and ATP, which are released under various pathophysiological conditions often associated with intracellular acidosis, could play an important role in the modulation of pHi under these conditions. Springer-Verlag, 1992 Bicarbonate-dependent transporter nationallicence Intracellular pH nationallicence α-adrenoceptor nationallicence ATP nationallicence Cardiomyocyte nationallicence Terzic André Division of Cardiovascular Diseases and Department of Pharmacology, Mayo Foundation, Guggenheim 7F, 55905, Rochester, MN, USA aut Pucéat Michel Laboratoire de Physiologie Cellulaire Cardiaque, Université Paris-Sud, INSERM U-241, F-91405, Orsay, France aut Clément-Chomienne Odile Laboratoire de Physiologie Cellulaire Cardiaque, Université Paris-Sud, INSERM U-241, F-91405, Orsay, France aut Vassort Guy Laboratoire de Physiologie Cellulaire Cardiaque, Université Paris-Sud, INSERM U-241, F-91405, Orsay, France aut Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 346/5(1992-11-01), 597-600 0028-1298 346:5<597 1992 346 210 https://doi.org/10.1007/BF00169019 text/html Onlinezugriff via DOI 1 brief-communication jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00169019 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Terzic André Division of Cardiovascular Diseases and Department of Pharmacology, Mayo Foundation, Guggenheim 7F, 55905, Rochester, MN, USA aut NATIONALLICENCE 700 1- Pucéat Michel Laboratoire de Physiologie Cellulaire Cardiaque, Université Paris-Sud, INSERM U-241, F-91405, Orsay, France aut NATIONALLICENCE 700 1- Clément-Chomienne Odile Laboratoire de Physiologie Cellulaire Cardiaque, Université Paris-Sud, INSERM U-241, F-91405, Orsay, France aut NATIONALLICENCE 700 1- Vassort Guy Laboratoire de Physiologie Cellulaire Cardiaque, Université Paris-Sud, INSERM U-241, F-91405, Orsay, France aut NATIONALLICENCE 773 0- Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 346/5(1992-11-01), 597-600 0028-1298 346:5<597 1992 346 210 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer