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Redox Regulation of Arterial L‐Type Calcium Channels
Author(s) -
Amberg Gregory C,
Frey Madeline M
Publication year - 2011
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.25.1_supplement.1026.5
Subject(s) - calcium , nadph oxidase , chemistry , voltage dependent calcium channel , t type calcium channel , biophysics , oxidase test , calcium channel , contraction (grammar) , reactive oxygen species , stimulation , biochemistry , microbiology and biotechnology , endocrinology , biology , enzyme , organic chemistry
Arterial walls are largely composed of smooth muscle cells. By contracting or relaxing, these cells regulate arterial diameter, thus influencing blood flow and blood pressure. The concentration of calcium in arterial smooth muscle largely determines the degree of arterial contraction. The main source of calcium entry into these cells is through voltage‐gated L‐type calcium channels. We recently reported that local NADPH oxidase‐mediated stimulation of PKC alpha‐dependent L‐type calcium channel activity (“calcium sparklets”) results in increased calcium influx and arterial contraction. However, details regarding the molecular mechanisms underlying redox‐dependent regulation of L‐type calcium channels are poorly understood. Using a combination of TIRF microscopy and patch clamp electrophysiology, here we investigate detailed aspects of redox‐dependent regulation of arterial L‐type calcium channels including experiments examining the molecular composition of the NADPH oxidase complex involved as well as determining the identity of the participating reactive oxygen species. Preliminary data suggest that Rac1‐dependent NADPH oxidase activity results in the generation of hydrogen peroxide that in turn stimulates PKC alpha‐dependent L‐type calcium channel function. This work was supported by the Pew Scholars Program (GCA).