Background/Aims: The roles of intercellular communication and T-type versus L-type voltage-dependent Ca2+ channels (VDCCs) in conducted vasoconstriction to local KCl-induced depolarization were investigated in mesenteric arterioles. Methods: Ratiometric Ca2+ imaging (R) using Fura-PE3 with micro-ejection of depolarizing KCl solution and VDCC blockers, and immunohistochemical and RT-PCR techniques were applied to isolated rat mesenteric terminal arterioles (n = 71 from 47 rats; intraluminal diameter: 24 ± 1 μm; length: 550-700 μm). Results: Local application of KCl (at 0 μm) led to local (ΔR = 0.54) and remote (ΔR = 0.17 at 500 μm) increases in intracellular Ca2+. Remote Ca2+ responses were inhibited by the gap junction uncouplers carbenoxolone and palmitoleic acid. CaV1.2, CaV3.1 and CaV3.2 channels were immunolocalized in vascular smooth muscle cells and Ca V3.2 in adjacent endothelial cells. Local and remote Ca2+ responses were inhibited by bath application of L- and T-type blockers [nifedipine, NNC 55-0396 and R(-)-efonidipine]. Remote Ca2+ responses (500 μm) were not affected by abolishing Ca2+ entry at an intermediate position on the arterioles (at 200-300 μm) using micro-application of VDCC blockers. Conclusion: Both L- and T-type channels mediate Ca2+ entry during conducted vasoconstriction to local KCl in mesenteric arterioles. However, these channels do not participate in the conduction process per se.
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine