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Am J Physiol Lung Cell Mol Physiol (September 6, 2002). doi:10.1152/ajplung.00023.2002
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Articles in PresS, published online ahead of print September 6, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00023.2002
Submitted on January 18, 2002
Accepted on September 4, 2002

Enhanced calcium signalling to bradykinin in airway smooth muscle from hyperresponsive inbred rats

Florence C. Tao, Saloni Shah, Amina A. Pradhan, Barbara Tolloczko, and James G. Martin1*

1 Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: james.martin{at}mcgill.ca.

Inbred Fisher 344 rats display airway hyperresponsiveness (AHR) in vivo compared with the normoresponsive Lewis strain. Fisher AHR has been linked with increased airway smooth muscle (ASM) contraction ex vivo and enhanced ASM cell intracellular Ca2+ mobilization in response to 5-HT compared to Lewis. To determine the generality of this association, we tested whether bradykinin (BK) also stimulates greater contraction of Fisher airways and greater Ca2+ mobilization in Fisher ASM cells. Explants of Fisher intraparenchymal airways constricted faster and to a greater degree in response to BK than Lewis airways. BK also evoked higher Ca2+ transients in Fisher than in Lewis ASM cells. ASM cell B2 receptor expression was similar between the two strains. BK activated both phosphatidylinositide-specific phospholipase C (PI-PLC) and phosphatidylcholine-specific phospholipase C (PC-PLC) to mobilize Ca2+ in Fisher and Lewis ASM cells. PI-PLC activity, as measured by inositol polyphosphate accumulation, was similar in the two strains. PKC inhibition with GF109203X, Go6973, or Go6983 attenuated BK-mediated Ca2+ transients in Fisher cells whereas GF109203X potentiated while Go6976 and Go6983 did not affect Ca2+ transients in Lewis cells. Enhanced Ca2+ mobilization in ASM cells can arise from variations in PKC and may be an important component of non-specific, innate airway hyperresponsiveness.




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