K⁺ channels in biological processes: vascular K⁺ channels in the regulation of blood pressure

Figures & data

Figure 1 Relationship between VSMC contraction and blood vessel diameter.

Notes: From a basal resting tone – and semi-contracted state – the VSMCs can either contract further, leading to a reduced blood vessel diameter and increased blood pressure, or relax, leading to a larger vessel diameter and reduced blood pressure. B, Basal resting tone, C, contraction, and R, relaxation of VSMCs.
Abbreviation: VSMC, vascular smooth muscle cell.

Figure 2 Modulation of membrane potential by K⁺ channels in vascular cells.

Notes: Endothelial cell: activation of K_Ca2.3/K_Ca3.1 channels in response to IP₃R-mediated Ca²⁺ release from the ER after receptor stimulation or in response to Ca²⁺ influx through TRP channels, and communication to adjacent smooth muscle cell via gap junctions and K_Ca2.3/K_Ca3.1 signaling. Smooth muscle cell: activation of K_ATP, K_V, VDCCs, and K₂P channels. Activation of BK_Ca channels by RyR-mediated Ca²⁺ sparks from the SR leads to hyperpolarization of the membrane potential and closure of VDCCs.
Abbreviations: ATP, adenosine triphosphate; BK_Ca, large-conductance Ca²⁺-activated K⁺ channel; ER, endoplasmic reticulum; IP₃, inositol 1,4,5-trisphosphate; IP₃R, IP₃ receptor; PLC, phospholipase C; PIP2, phosphatidyl-inositol-bisphosphate; K₂P, two-pore domain K⁺ channel; K_ATP, ATP-sensitive K⁺; K_Ca, Ca²⁺-activated K⁺ channel; K_V, voltage-gated K⁺ channel; RyR, ryanodine receptor; SR, sarcoplasmic reticulum; TRP, transient receptor potential; VDCC, voltage-dependent Ca²⁺ channel.