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Cardiovascular Research 2002 55(2):233-235; doi:10.1016/S0008-6363(02)00464-9
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Is Kv channel inhibition a common path to hypoxic pulmonary vasoconstriction?

Insuk So and Yung E Earm*

Department of Physiology and Biophysics, and National Research Laboratory for Cellular Signalling, Seoul National University College of Medicine, 28 Yonkeun-Dong, Chongno-Ku, Seoul 110-799, South Korea

* Corresponding author. Tel.: +82-2-740-8224; fax: +82-2-763-9667 earmye@snu.ac.kr

Received 3 May 2002; accepted 3 May 2002

The first 10% of the full text of this article appears below.

See article by Hogg et al. [1] (pages 349–360) in this issue.


   1. Kv channels and hypoxic pulmonary vasoconstriction
 
Hypoxic pulmonary vasoconstriction (HPV), a vasomotor mechanism that matches regional perfusion to ventilation, is initiated by depolarization of the membrane potential of pulmonary arterial smooth muscle cells (PASMC). There are still many debates as to which factor(s) is(are) responsible to induce membrane depolarization [2]. Voltage-gated potassium channel (Kv), calcium-activated potassium channel (KCa), release of intracellular calcium, change of intracellular redox potential or other factors are candidates. However, the most probable candidate for membrane depolarization so far is the inhibition of voltage-gated potassium channels (Kv) which leads to opening of voltage-gated calcium channels, and . . . [Full Text of this Article]


   2. Kv1.5 vs. Kv2.1
 

   3. Do Kv channels need O2 sensor?
 

   4. Other channels or factors?
 

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