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Dynamic turnover of L‐type calcium channels in rat mesenteric arteries in vivo
Author(s) -
Srivastava Anup Kumar,
Kharade Sujay V,
Fletcher Terry W,
Rhee Sung,
Rusch Nancy J
Publication year - 2012
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.26.1_supplement.1115.16
Subject(s) - in vivo , mesenteric arteries , chemistry , calcium channel , endocrinology , medicine , puromycin , vasoconstriction , l type calcium channel , anatomy , voltage dependent calcium channel , artery , calcium , biology , biochemistry , protein biosynthesis , microbiology and biotechnology
Increased Ca2+‐dependent vascular tone is a hallmark feature of hypertension. The upregulation of the pore‐forming α 1C subunit of the voltage‐gated L‐type Ca2+ (Ca L ) channel contributes to this increased Ca2+‐dependent tone. However, the mechanism by which high blood pressure drives Ca L channel expression has been difficult to identify and may require monitoring Ca L channel turnover in arteries in vivo . To enable these studies, we anesthetized Sprague‐Dawley rats with isoflurane and exposed intestinal loops containing mesenteric arteries (MA) through a minimal abdominal opening. Distal MA branches were removed immediately (0 hr). Then the MA bed was pinned flat in a silicone chamber and exposed either to physiological salt solution (PSS, control) or PSS + 20 μg/ml puromycin to inhibit de novo protein synthesis. After 6 hr, the exposed branches of the MA bed were removed. Western blots compared the expression of the Ca L channel α 1C pore protein between 0 and 6 hr. The immunoreactive band corresponding to α 1C was maintained in MA exposed to PSS alone but reduced by 75% in MA exposed to puromycin. Thus, vascular Ca L channel turnover is rapid at normal blood pressure levels, raising the possibility that reduced turnover during hypertension could increase Ca L channel abundance. Funded by NIH R01 HL064806 (NJR)