Figure 2.

Spatial distribution and functions of calcium-activated potassium channels in the vascular wall. SK_Ca (SK3) and IK_Ca (IK1) are preferentially expressed in ECs. SK_Ca are preferentially located in caveolin-rich domains, at sites of homocellular endothelial gap junctions. A global increase in endothelial [Ca²⁺]_i preferentially activates SK_Ca and an EDHF-mediated response involving a Cx-dependent pathway (Dora et al., 2008). IK_Ca are preferentially localized at the sites of endothelial projections towards the underlying smooth muscle cells. Co-localized sarcoplasmic reticulum elements and associated local calcium release (calcium pulsar) regulate IK1 activation and vascular tone via potassium efflux and subsequent activation of smooth muscle Na⁺/K⁺-ATPase (Ledoux et al., 2008b). The activation of these two channels also favours calcium entry, amplifying NO production (Stankevicius et al., 2006). When BK_Ca channels are expressed in the ECs they can also contribute to this latter mechanism (Brakemeier et al., 2003). BK_Ca are preferentially expressed in smooth muscle cells and are often clustered in large groups. They are activated by calcium sparks or following a global increase in smooth muscle [Ca²⁺]_i. They generate STOCs, leading to arterial smooth muscle hyperpolarization and relaxation (Perez et al., 1999). IK_Ca are expressed in VSMCs undergoing de-differentiation and are involved in their proliferation (Neylon et al., 1999). BK_Ca, calcium-activated potassium channels of large conductance; Cx, connexin; EC, endothelial cell; EDCF, endothelium-derived contracting factor; eNOS, endothelial nitric oxide synthase; IK_Ca, calcium-activated potassium channels of intermediate conductance; IP₃R, IP₃ recepteur; Kir, inwardly rectifying potassium channel; NO, nitric oxide; RyR, ryanodine receptor; SK_Ca, calcium-activated potassium channels of small conductance; STOCs, spontaneous transient outward currents; TRPV4, vanilloid transient receptor potential channel 4; VSMC, vascular smooth muscle cell.