期刊
MICROCIRCULATION
卷 13, 期 2, 页码 119-130出版社
WILEY
DOI: 10.1080/10739680500466400
关键词
calcium; Ca2+-activated K+ channel; EDHF; endothelial cell
资金
- NHLBI NIH HHS [HL-51055] Funding Source: Medline
- NIGMS NIH HHS [GM-31278] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
Objective: The authors probed endothelium-dependent dilation and endothelial cell Ca2+ handling in myogenically active resistance arteries. Methods: First-order arteries were removed from rat cremaster muscles, cannulated, and pressurized (75 mmHg). Vessel diameter and endothelial cell Ca2+ were monitored using confocal microscopy, and arterial ultrastructure was determined using electron microscopy. Results: Acetylcholine (ACh) stimulated elevations and oscillations in endothelial cell Ca2+, and concentration-dependently dilated arteries with myogenic tone. NO-independent dilation was blocked by 35 mM K+. Combined IKCa (1 mu M TRAM-34) and SKCa (100 nM apamin) blockade partially inhibited NO-independent relaxations, with residual relaxations sensitive to BKCa or cytochrome P-450 inhibition (100 nM iberiotoxin, and 20 mu M 17-ODYA or 10 mu M MS-PPOH). 11,12-EET stimulated iberiotoxin-sensitive dilation, but did not affect endothelial cell Ca2+. 15 mM K+ evoked dilation sensitive to inhibition of K-IR (30 mu M Ba2+) and Na+/K+-ATPase (10 mu M ouabain), whereas these blockers did not affect ACh-mediated dilations. Homo-and heterocellular gap junctions were identified in radial sections through arteries. Conclusion: These data suggest that rises in endothelial cell Ca2+ stimulate SKCa and IKCa channels, leading to hyperpolarization and dilation, likely due to electrical coupling. In addition, a component was unmasked following SKCa and IKCa blockade, attributable to activation of BKCa channels by cytochrome P-450 metabolites.
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