Skip Navigation

Cardiovascular Research 1998 37(1):179-186; doi:10.1016/S0008-6363(97)00203-4
© 1998 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Yamaguchi, S.
Right arrow Articles by Haruaki Nakaya,
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yamaguchi, S.
Right arrow Articles by Haruaki Nakaya,
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1998, European Society of Cardiology

Selective impairment of HCO3–-dependent pHi regulation by lysophosphatidylcholine in guinea pig ventricular myocardium

Seiichi Yamaguchi, Masaji Tamagawa, Nobuyuki Nakajima and Haruaki Nakaya*

Department of Pharmacology and First Department of Surgery, Chiba University School of Medicine, Chiba 260, Japan

* Corresponding author. Tel. (+81-43) 2262050; Fax (+81-43) 2262052, E-mail: nakaya@med.m.chiba-u.ac.jp

Objective: The aim was to examine the effects of lysophosphatidylcholine (LPC), an amphiphilic lipid metabolite in ischemic myocardium, on intracellular pH (pHi) regulatory systems in guinea pig papillary muscles. Methods: In CO2/HCO3–-buffered Tyrode solution, pHi, intracellular Na+ activity (aNai) and membrane potential of isolated guinea pig papillary muscles were measured using ion-selective microelectrode and conventional microelectrode. Standard ammonium prepulsing with 20 mM NH4Cl was used to produce an intracellular acid load, and effects of LPC on the pHi recovery from acidosis were evaluated in the absence and presence of a transport inhibitor. Results: LPC acidified the resting pHi by 0.03±0.01 pH units (n = 15, P<0.01) concomitantly with a slight decrease in resting membrane potential and an increase in aNai in quiescent preparations. The pHi recovery rate from an intracellular acid load was decreased to 83±4% of the control value by 30 µM LPC (n = 8, P<0.05) but not by 30 µM phosphatidylcholine (PC). In the presence of 10 µM 5-(N,N–hexamethylene) amiloride (HMA), a Na+–H+ exchange inhibitor, LPC still slowed pHi recovery from an intracellular acid load to 77±4% of the control (n = 5, P<0.05). However, LPC failed to alter the pHi recovery rate in the presence of 4,4'-diisothiocyanatostilbene–2,2'-disulfonic acid (DIDS, 0.5 mM), a Na+-HCO3– symport inhibitor. Conclusion: LPC impairs Na+–HCO3– symport but not Na+–H+ exchange, and LPC may potentiate its arrhythmogenic action by intensifying the intracellular acidosis in ischemic myocardium.

KEYWORDS Lysophosphatidylcholine; Guinea pig papillary muscles; Intracellular pH; Intracellular Na+ activity; Na+–H+ exchange; Na+–HCO3– symport; Ion-selective microelectrode


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Physiol. Rev.Home page
E. Carmeliet
Cardiac Ionic Currents and Acute Ischemia: From Channels to Arrhythmias
Physiol Rev, July 1, 1999; 79(3): 917 - 1017.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.