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Regulation of Pulmonary Microvascular Endothelial Cell Cyclic Adenosine Monophosphate by Adenylyl Cyclase*: Implications for Endothelial Barrier Function

Troy Stevens, PhD; W.J. Thompson
Author and Funding Information

*From the Department of Pharmacology, University of South Alabama College of Medicine, Mobile, AL.

Correspondence to: Troy Stevens, PhD, Department of Pharmacology, University of South Alabama College of Medicine, MSB 3130, Mobile, AL 36688-0002



Chest. 1999;116(suppl_1):32S-33S. doi:10.1378/chest.116.suppl_1.32S-a
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Extract

Pulmonary microvascular endothelial cells (PMVECs) form a more restrictive barrier to solute and macromolecular transfer than do pulmonary artery endothelial cells (PAECs), although mechanisms responsible for enhanced barrier properties in PMVECs are unknown. Recent studies in PAECs indicate inflammatory mediators that stimulate store-operated Ca2+ entry decrease cyclic adenosine monophosphate (cAMP) content due to Ca2+ inhibition of adenylyl cyclase activity, an effect that promotes barrier disruption. PMVECs similarly express a Ca2+-inhibited adenylyl cyclase but basal and agonist-evoked Ca2+ entry is reduced in these cells compared with PAECs. Present studies therefore examined the role of store-operated Ca2+ entry in regulation of PMVEC adenylyl cyclase activity and cAMP content.


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