Mechanical stimulation induces Ca2+i transients and membrane depolarization in cultured endothelial cells. Effects on Ca2+i in co-perfused smooth muscle cells

Cytosolic Ca²⁺ concentration and membrane potential were monitored in individual cultured enothelial cells mechanically stimulated with a micropipette attached to the stage of a microscope. Both dimpling and poking of endothelial cells resulted in Ca²⁺_i transients (from 63 ± 12 to 397 ± 52 nM, characterized by a refractory period of approx. 2 min) and cell depolarization. Ca²⁺_i transients of the reduced amplitude (201 ± 41 nM) were evoked by mechanical stimulation of endothelial cells incubated in a Ca²⁺-free medium. Dimpling-induced Ca²⁺_i transients were refractory to the pretreatments with pertussis toxin, colchicine, or cytochalasin B, and were not mimicked by an increase in the hydrodynamic pressure. In a co-perfusion system (endothelium: smooth muscle), both the KCl-induced depolarization and ionomycin-induced increase in Ca²⁺_i in the endothelial cells resulted in the reduction of Ca²⁺_i in the smooth muscle cells. The data reported are consistent with the phenomenon of vascular relaxation in response to the increased blood flow. We hypothesize that the mechanical interaction of the formed elements with the microvascular endothelium can serve as a pacemaker for the sustained relaxation of vascular smooth muscle.