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Vascular smooth muscle contraction is suppressed by feedback dilation mediated by the endothelium. In skeletal muscle arterioles, this feedback can be activated by Ca 2+ signals passing from smooth muscle through gap junctions to endothelial cells, which protrude through holes in the internal elastic lamina to make contact with vascular smooth muscle cells. Although hypothetically either Ca 2+ or inositol trisphosphate (IP 3 ) may provide the intercellular signal, it is generally thought that IP 3 diffusion is responsible. We provide evidence that Ca 2+ entry through L-type voltage-dependent Ca 2+ channels (VDCCs) in vascular smooth muscle can pass to the endothelium through positions aligned with holes in the internal elastic lamina in amounts sufficient to activate endothelial cell Ca 2+ signaling. In endothelial cells in which IP 3 receptors (IP 3 Rs) were blocked, VDCC-driven Ca 2+ events were transient and localized to the endothelium that protrudes through the internal elastic lamina to contact vascular smooth muscle cells. In endothelial cells in which IP 3 Rs were not blocked, VDCC-driven Ca 2+ events in endothelial cells were amplified to form propagating waves. These waves activated voltage-insensitive, intermediate-conductance, Ca 2+ -activated K + (IK Ca ) channels, thereby providing feedback that effectively suppressed vasoconstriction and enabled cycles of constriction and dilation called vasomotion. Thus, agonists that stimulate vascular smooth muscle depolarization provide Ca 2+ to endothelial cells to activate a feedback circuit that protects tissue blood flow.

Voltage-dependent Ca 2+ entry into smooth muscle during contraction promotes endothelium-mediated feedback vasodilation in arterioles

Voltage-dependent Ca ²⁺ entry into smooth muscle during contraction promotes endothelium-mediated feedback vasodilation in arterioles