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Am J Physiol Lung Cell Mol Physiol (February 3, 2006). doi:10.1152/ajplung.00494.2005
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Submitted on November 21, 2005
Accepted on January 30, 2006

Modulation of the Ca2+ sensitivity of airway smooth muscle cells in murine lung slices

Yan Bai1 and Michael J Sanderson1*

1 Department of Physiology, UMASS Medical School, Worcester, MA, USA

* To whom correspondence should be addressed. E-mail: Michael.Sanderson{at}umassmed.edu.

To investigate the phenomenon of Ca2+ sensitization, we developed a new intact airway and arteriole smooth muscle cell (SMC) "model" by treating murine lung slices with ryanodine-receptor antagonist, ryanodine (50 µM) and caffeine (20 mM). A sustained elevation in intracellular Ca2+ concentration ([Ca2+]i) was induced in both SMC types by the ryanodine/caffeine treatment due to the depletion of internal Ca2+ stores and the resulting persistent influx of Ca2+. Arterioles responded to this sustained increase in [Ca2+]i with a sustained contraction. By contrast, airways responded to sustained high [Ca2+]i with a transient contraction followed by relaxation. Subsequent exposure to methacholine (MCh) induced a sustained concentration-dependent contraction of the airway without a change in the [Ca2+]i. During sustained MCh-induced contraction, Y-27632 (a Rho kinase inhibitor) and GF109203X (a protein kinase C inhibitor) induced a concentration-dependent relaxation without changing the [Ca2+]i. The cAMP elevating agents, forskolin (an adenylyl cyclase activator), IBMX (a phosphodiesterase inhibitor) and caffeine (also acting as a phosphodiesterase inhibitor) exerted similar relaxing effects. These results indicate that (a) ryanodine/caffeine treatment is a valuable tool for investigating the contractile mechanisms of SMCs while avoiding non-specific effects due to cell permeabilization, (b) in the absence of agonist, sustained high [Ca2+]i has a differential time-dependent effect on the Ca2+ sensitivity of airway and arteriole SMCs, (c) MCh facilitates the contraction of airway SMCs by inducing Ca2+ sensitization via the activation of Rho-kinase and protein kinase C, and (d) cAMP elevating agents contribute to the relaxation of airway SMCs through Ca2+ desensitization.




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