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Articles in PresS, published online ahead of print July 12, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00345.2001
Submitted on August 27, 2001
Accepted on July 8, 2002
-Adrenoreceptor Mediated Pulmonary Artery Smooth Muscle Contraction
1 Center for Anesthesiology Research, The Cleveland Clinic Foundation, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: murrayp{at}ccf.org.
Our objectives were to identify the relative contributions of intracellular free Ca2+ concentration ([Ca2+]i) and myofilament Ca2+ sensitivity in the pulmonary artery smooth muscle(PASM) contractile response to the -adrenoreceptor agonist, phenylephrine (PE), and to assess the role of protein kinase C (PKC), tyrosine kinases (TK) and Rho-kinase (ROK) in that response. Our hypothesis was that multiple signaling pathways are involved in the regulation of [Ca2+]i, myofilament Ca2+ sensitization and vasomotor tone in response to -adrenoreceptor stimulation of PASM. Simultaneous measurement of [Ca2+]i and isometric tension was performed in isolated canine pulmonary arterial strips loaded with fura-2/AM. PE-induced tension development was due to sarcolemmal Ca2+ influx, Ca2+ release from IP3-dependent sarcoplasmic reticulum Ca2+ stores and myofilament Ca2+ sensitization. Inhibition of either PKC or TK partially attenuated the sarcolemmal Ca2+ influx component and the myofilament Ca2+ sensitizing effect of PE. Combined inhibition of PKC and TK did not have an additive attenuating effect on PE-induced Ca2+ sensitization. ROK inhibition slightly decreased [Ca2+]i, but completely inhibited myofilament Ca2+ sensitization. These results indicate that PKC and TK activation positively regulate sarcolemmal Ca2+ influx in response to -adrenoreceptor stimulation in PASM, but have relatively minor effects on myofilament Ca2+ sensitivity. Rho-kinase is the predominant pathway mediating PE-induced myofilament Ca2+ sensitization.
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