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L‐type Ca 2+ (Ca L ) Channels are Silent During Depolarization of Venous Smooth Muscle
Author(s) -
Thakali Keshari,
Kharade Sujay V,
Rhee Sung W,
Rusch Nancy J
Publication year - 2010
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.24.1_supplement.576.1
Subject(s) - depolarization , nifedipine , biophysics , chemistry , constriction , diastolic depolarization , calcium , hyperpolarization (physics) , vascular smooth muscle , l type calcium channel , anatomy , voltage dependent calcium channel , medicine , smooth muscle , biology , stereochemistry , heart rate , organic chemistry , sinoatrial node , nuclear magnetic resonance spectroscopy , blood pressure
Calcium channel blockers (CCBs) reduce cardiac afterload but not preload, suggesting that the venous circulation is insensitive to their dilator action. Indeed we observed that CCBs prevent KCl‐induced constriction in pressurized rat mesenteric arteries (MA) but not veins (MV), suggesting that Ca L channels are silent during depolarization of venous smooth muscle cells (SMCs). In patch‐clamp studies, single Ca L channel currents in cell‐attached patches were abundant during depolarization from −70 mV to −10 mV in SMCs of MA (NP o = 0.26±0.05) but rarely occurred in MV (NP o =0.02±0.01). Calcium imaging in fluo‐4 loaded vessel segments revealed that KCl (60mM)‐induced depolarization similarly increased intracellular Ca 2+ ([Ca] i ) in MA and MV by 74% and 66%, respectively. However, whereas the CCB nifedipine (10 μM) blocked KCl‐induced constriction in MA and [Ca] i failed to rise, nifedipine failed to reduce KCl‐induced constrictions in MV and [Ca] i still increased by 34%. Our results suggest that Ca L channels fail to open during depolarization of MV and an alternative source of activator Ca 2+ mediates KCl‐induced constriction. Work supported by NIH NRSA 1F32 HL095284