Abstract
1. The molecular identity of the K channels giving rise to the negative membrane potential of pulmonary artery smooth muscle cells has yet to be determined. 2. To date, most studies have focused on voltage-gated, delayed rectifier channels and their roles in mediating hypoxia-induced membrane depolarization. There is, however, strong evidence that an outwardly rectifying K+ conductance distinct from the classical delayed rectifier is involved. 3. Growing evidence that TASK-like channels can sense hypoxia and are present in pulmonary artery smooth muscle cells suggests that they may be responsible for the resting K+ conductance and resting potential. 4. The present review considers the evidence that particular K channels maintain the resting membrane potential of pulmonary artery smooth muscle cells and mediate the depolarizing response to hypoxia.
Original language | English |
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Article number | 11985545 |
Pages (from-to) | 330-333 |
Number of pages | 4 |
Journal | Clinical and Experimental Pharmacology and Physiology |
Volume | 29 |
Issue number | 4 |
Early online date | 5 Mar 2002 |
DOIs | |
Publication status | Published - Apr 2002 |
Keywords
- hypoxia
- pulmonary artery
- smooth muscle
- vasoconstriction
- two-pore domain acid-sentitive K channels
- resting potential
- pulmonary hypertension
- membrane potential
- K channel
- Kv