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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 IK(Ca) (1 microM TRAM-34) and SK(Ca) (100 nM apamin) blockade partially inhibited NO-independent relaxations, with residual relaxations sensitive to BK(Ca) or cytochrome P-450 inhibition (100 nM iberiotoxin, and 20 microM 17-ODYA or 10 microM 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 microM Ba2+) and Na+/K+-ATPase (10 microM 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 SK(Ca) and IK(Ca) channels, leading to hyperpolarization and dilation, likely due to electrical coupling. In addition, a component was unmasked following SK(Ca) and IK(Ca) blockade, attributable to activation of BK(Ca) channels by cytochrome P-450 metabolites.

Original publication




Journal article



Publication Date





119 - 130


Acetylcholine, Animals, Arteries, Calcium, Calcium Signaling, Dose-Response Relationship, Drug, Endothelium, Vascular, Enzyme Inhibitors, Gap Junctions, Male, Muscle, Smooth, Vascular, Potassium Channels, Calcium-Activated, Rats, Rats, Wistar, Sodium-Potassium-Exchanging ATPase, Vasodilation, Vasodilator Agents