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Ryanodine receptors decant internal Ca²⁺ store in human and bovine airway smooth muscle

¹ Firestone Institute for Respiratory Health, St Joseph’s Hospital, ² Dept of Medicine, McMaster , University, Hamilton, and ³ Toronto Lung Transplant Program, Division of Thoracic Surgery, University of Toronto, ON, Canada.

CORRESPONDENCE: L. J. Janssen, L-314, St Joseph’s Hospital, 50 Charlton Avenue East, Hamilton, ON, Canada L8N 4A6. Fax: 1 9055406510. E-mail: janssenl{at}mcmaster.ca

Keywords: Airway smooth muscle, Ca²⁺-handling, excitation–contraction coupling, ryanodine receptors

Received: December 11, 2007
Accepted February 29, 2008

Several putative roles for ryanodine receptors (RyR) were investigated in human and bovine airway smooth muscle.

Changes in intracellular Ca²⁺ concentration ([Ca²⁺]_i) and membrane current were investigated in single cells by confocal fluorimetry and patch-clamp electrophysiology, respectively, whereas mechanical activity was monitored in intact strips with force transducers.

RyR released Ca²⁺ from the sarcoplasmic reticulum in a ryanodine- and chloroethyl phenol (CEP)-sensitive fashion. Neither ryanodine nor CEP inhibited responses to KCl, cholinergic agonists or serotonin, indicating no direct role for RyR in contraction; in fact, there was some augmentation of these responses. In tissues pre-contracted with carbachol, the concentration–response relationships for isoproterenol and salmeterol were unaffected by ryanodine; relaxations due to a nitric oxide donor were also largely unaffected. Finally, it was examined whether RyR were involved in regulating [Ca²⁺]_i within the subplasmalemmal space using patch-clamp electrophysiology as well as Ca²⁺ fluorimetry: isoproterenol increased [Ca²⁺]_i- and Ca²⁺-dependent K⁺ current activity in a ryanodine-sensitive fashion.

In conclusion, ryanodine receptors in airway smooth muscle are not important in directly mediating contraction or relaxation. The current authors speculate instead that these allow the sarcoplasmic reticulum to release Ca²⁺ towards the plasmalemma (to unload an overly full Ca²⁺ store and/or increase the Ca²⁺-buffering capacity of the sarcoplasmic reticulum) without affecting bronchomotor tone.