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Mechanisms underlying smooth muscle Ca 2+ waves in cremaster muscle arterioles
Author(s) -
Ella Srikanth Reddy,
Davis Michael J,
Meininger Gerald A,
Yang Yan,
Dora Kim A,
Hill Michael A
Publication year - 2009
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.23.1_supplement.767.8
Subject(s) - cyclopiazonic acid , ryanodine receptor , vascular smooth muscle , biophysics , vasoconstriction , chemistry , endoplasmic reticulum , myogenic contraction , medicine , anatomy , smooth muscle , biology , biochemistry
Vascular smooth muscle cells (VSMC) exhibit a number of spatially and temporally restricted Ca 2+ signals including sparks, waves, flashes and sparklets. In the present studies Ca 2+ waves were measured in VSMC of myogenically active rat arterioles with an aim to understand their mechanism and relationship to mechanical forces. Waves were measured in Fluo‐4 loaded VSMC via high‐speed confocal imaging. The number of cells exhibiting waves and their frequency increased linearly with increasing intraluminal pressure. Ca 2+ waves persisted despite inhibition of myogenic tone by nifedipine (1µM), adenosine (10µM) and ML7 (10µM). Ryanodine (10µM), 2APB (30µM) a putative IP 3 receptor blocker, and cyclopiazonic acid (CPA; 30µM) abolished Ca 2+ waves with a critical role of the sarcoplasmic reticulum (SR). Ryanodine and CPA caused vasoconstriction while 2APB caused dilation. Thus, Ca 2+ waves are not dependent on active myogenic constriction but are influenced by pressure‐induced distention/tension and cyclic release/uptake of Ca 2+ by the SR. Collectively, the data are consistent with mechanical force impacting on the Ca 2+ filling state of the SR prior to pressure‐dependent opening of voltage‐gated Ca 2+ channels.