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- Title
BK channel β1 subunits regulate airway contraction secondary to M2 muscarinic acetylcholine receptor mediated depolarization.
- Authors
Semenov, Iurii; Wang, Bin; Herlihy, Jeremiah T.; Brenner, Robert
- Abstract
Parasympathetic nerve activation of M3 and M2 muscarinic acetylcholine receptors initiates and modulates calcium release from the sarcoplasmic reticulum to control airway smooth muscle contraction. Here we investigate M2 acetylcholine receptors that also contribute to contraction through depolarization and recruitment of voltage-dependent calcium channels (VDCCs). We find that the calcium- and voltage-activated potassium channel (BK channel) and its β1 accessory subunit are important proteins that oppose M2-mediated contraction of airway smooth muscle. BK channels contribute to a negative baseline membrane voltage from which M2-mediated depolarization only weakly activates VDCCs. The role of BK β1 to oppose M2 signalling is evidenced by a greater than fourfold increase in the contribution of L-type VDCCs to contraction that otherwise does not occur with M2 receptor antagonist or with β1 containing BK channels. These findings provide a better understanding of how cholinergic second messenger signalling impinges on voltage-dependent mechanisms and excitation-contraction coupling of smooth muscle.
- Publication
Journal of Physiology, 2011, Vol 589, Issue 7, p1803
- ISSN
0022-3751
- Publication type
Article
- DOI
10.1113/jphysiol.2010.204347