Skip Navigation

Cardiovascular Research 2003 58(1):76-88; doi:10.1016/S0008-6363(02)00858-1
© 2003 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 Volk, T.
Right arrow Articles by Ehmke, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Volk, T.
Right arrow Articles by Ehmke, H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

A polycystin-2-like large conductance cation channel in rat left ventricular myocytes

Tilmann Volk*, Alexander Peter Schwoerer, Susanne Thiessen, Jobst-Hendrik Schultz and Heimo Ehmke*

Institut für Physiologie, Universitätskrankenhaus Hamburg-Eppendorf, Universität Hamburg, Martinistraße 52, 20246 Hamburg, Germany ehmke{at}uke.uni-hamburg.de

* Corresponding authors. Tel.: +49-40-42803-9615 (T. Volk); +49-40-42803-3183 (H. Ehmke); fax: +49-40-42803-9299. volk{at}uke.uni-hamburg.de

Objective: Several members of the PKD gene family (PKD2, PKDL and PKD2L2) are expressed in the heart. Polycystin-2 and its homologues, which are encoded by these genes, have recently been shown to form Ca2+-regulated nonselective cation channels in heterologous expression systems. Previously, large conductance nonselective cation channels (LCC) have been described in cardiomyocytes, however, their molecular identity remained obscure. We therefore examined whether LCCs may be formed by polycystins. Methods: Myocytes isolated from the rat left ventricle were investigated by the whole-cell patch-clamp technique and single-cell RT-PCR. Results: Application of 10 mM caffeine to the bath solution to increase the intracellular Ca2+ concentration led to activation of LCC in 56% of the myocytes investigated (total n = 651), in ~10%, more than three LCCs were detected. The single channel conductance was ~300 pS for monovalent cations and the channel was relatively nonselective for the monovalent cations Na+, K+, Li+, and Cs+ and also permeable for the divalent cations Ca2+ and Ba2+, but impermeable for NMDG+ and Cl–. Amiloride (IC50=131±1.1 µM) and millimolar concentrations of the trivalent cations Gd3+ and La3+ inhibited the LCC. Single-cell RT-PCR analysis revealed that mRNA of PKD2 and PKD2L2, but not PKDL or PKD1 are expressed in individual rat left ventricular myocytes. Conclusion: The characteristics of LCC shown in the present study are nearly identical to those observed for polycystin-2 and its homologues suggesting that polycystin-2 or polycystin-2L2 underlie LCC in ventricular myocytes.

KEYWORDS Ca-channel; Calcium (cellular); Ion channels; Myocytes; Na channel; Single channel currents


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
 Am. J. Physiol. Heart Circ. Physiol.Home page
Y.-a. Zhang, R. A. Tuft, L. M. Lifshitz, K. E. Fogarty, J. J. Singer, and H. Zou
Caffeine-activated large-conductance plasma membrane cation channels in cardiac myocytes: characteristics and significance
Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2448 - H2461.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
G. I. Anyatonwu, M. Estrada, X. Tian, S. Somlo, and B. E. Ehrlich
Regulation of ryanodine receptor-dependent calcium signaling by polycystin-2
PNAS, April 10, 2007; 104(15): 6454 - 6459.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
R. Inoue, L. J. Jensen, J. Shi, H. Morita, M. Nishida, A. Honda, and Y. Ito
Transient Receptor Potential Channels in Cardiovascular Function and Disease
Circ. Res., July 21, 2006; 99(2): 119 - 131.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
B. Pelucchi, G. Aguiari, A. Pignatelli, E. Manzati, R. Witzgall, L. del Senno, and O. Belluzzi
Nonspecific Cation Current Associated with Native Polycystin-2 in HEK-293 Cells
J. Am. Soc. Nephrol., February 1, 2006; 17(2): 388 - 397.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
K. Hackmann, A. Markoff, F. Qian, N. Bogdanova, G. G. Germino, P. Pennekamp, B. Dworniczak, J. Horst, and V. Gerke
A splice form of polycystin-2, lacking exon 7, does not interact with polycystin-1
Hum. Mol. Genet., November 1, 2005; 14(21): 3249 - 3262.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
M. Murakami, T. Ohba, F. Xu, S. Shida, E. Satoh, K. Ono, I. Miyoshi, H. Watanabe, H. Ito, and T. Iijima
Genomic Organization and Functional Analysis of Murine PKD2L1
J. Biol. Chem., February 18, 2005; 280(7): 5626 - 5635.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
A. Gwanyanya, B. Amuzescu, S. I. Zakharov, R. Macianskiene, K. R. Sipido, V. M. Bolotina, J. Vereecke, and K. Mubagwa
Magnesium-inhibited, TRPM6/7-like channel in cardiac myocytes: permeation of divalent cations and pH-mediated regulation
J. Physiol., September 15, 2004; 559(3): 761 - 776.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
H. F. Cantiello
Regulation of calcium signaling by polycystin-2
Am J Physiol Renal Physiol, June 1, 2004; 286(6): F1012 - F1029.
[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.