Skip Navigation

Cardiovascular Research 2002 55(2):349-360; doi:10.1016/S0008-6363(02)00411-X
© 2002 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 Hogg, D. S
Right arrow Articles by Kozlowski, R. Z
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hogg, D. S
Right arrow Articles by Kozlowski, R. Z
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

KV2.1 channels mediate hypoxic inhibition of IKV in native pulmonary arterial smooth muscle cells of the rat

Dayle S Hogga, Andrew R.L Daviesa, Gordon McMurrayb and Roland Z Kozlowskia,*

aDepartment of Pharmacology, School of Medical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK
bUniversity Department of Pharmacology, Mansfield Road, Oxford OX1 3QT, UK

* Corresponding author. Tel.: +44-117-954-6875; fax: +44-117-925-2659 roland.kozlowski{at}bristol.ac.uk

Objective: To determine whether, in native pulmonary arterial smooth muscle cells (PASMC), KV2.1 delayed-rectifying K+ channels are central to the process of hypoxic pulmonary vasoconstriction. Methods: In this study, we tested for the presence of KV2.1 channel transcripts in rat small pulmonary arteries using RT-PCR, and for the protein itself using immunolocalisation. The contribution of KV2.1 channels to whole-cell KV currents (IKV) and their role in hypoxic inhibition of IKV in native PASMC was investigated utilising patch-clamp recordings. Results: KV2.1 mRNA expression and AbKV2.1 (anti-KV2.1 antibody) protein immunoreactivity were both present in small pulmonary arteries. Dialysis of PASMC with AbKV2.1 significantly attenuated IKV by 67% at +50 mV. Hypoxia (~20–30 mmHg) inhibited IKV by ~70% at +50 mV. Ablation of currents associated with KV2.1 using AbKV2.1 caused a marked reduction in the amplitude of IKV. Hypoxia in the presence of the antibody did not affect the magnitude of IKV. Conclusions: These results indicate that KV2.1 channel subunits exist within small pulmonary arteries and conduct a significant part of IKV within native PASMC. Furthermore, application of AbKV2.1 abolishes hypoxic inhibition of IKV in native PASMC suggesting that KV2.1 channels play a pivotal role in mediating hypoxic pulmonary vasoconstriction.

KEYWORDS Arteries; Hypoxia/anoxia; K-channel; Myocytes; Pulmonary circulation


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




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.