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Phosphatidylcholine‐specific PLC plays a central role in the development of myogenic tone in murine resistance arteries (546.4)
Author(s) -
Mauban Joseph,
Zacharia Joseph,
Fairfax Seth,
Wier W
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.546.4
Subject(s) - myogenic contraction , ryanodine receptor , phospholipase c , mesenteric arteries , microbiology and biotechnology , receptor , chemistry , signal transduction , medicine , endocrinology , biology , artery , biochemistry , smooth muscle
The Bayliss mechanism posits that an increase in transmural pressure causes an artery to contract in response to distending pressure. Previous studies have established that PLC is critical for the myogenic response. However, the functional type/s of phospholipase C (PI‐PLC or PC‐PLC) involved and actions of PLC second messenger products (IP 3 , DAG) have not been clarified. This study of myogenic tone was therefore carried out to 1) identify the functional type/s of PLC involved and 2) investigate the role of IP 3 and IP 3 ‐induced Ca 2+ release, in the maintenance of myogenic constriction. Pressurized mesenteric arteries showed that inhibition of phosphoinositide‐specific PLC with Edelfosine, surprisingly,increases myogenic tone at physiological pressures. In contrast, inhibition of phosphatidylcholine‐specific PLC with D609 abolishes myogenic tone. The Bayliss mechanism therefore involves a hitherto unrecognized role for the cleavage of phosphatidylcholine and formation of DAG. Ca 2+ waves are virtually absent in myogenically active arteries. In addition, 1) SR Ca 2+ release via IP 3 and ryanodine receptors, and 2) Ca 2+ store emptying, all do not eliminate myogenic constriction. In summary, the Bayliss mechanism signaling cascade in murine mesenteric resistance arteries does not require 1) sustained IP 3 formation, 2) or Ca 2+ release from SR stores via ryanodine and IP 3 receptors. Instead, the signaling cascade critically requires PLC cleavage of phosphatidylcholine. Grant Funding Source : Supported by NHLBI RO1091969 and NIH T32HL072751