Fig. 8

Putative model of vasomotion phenomenon in rat blood vessels. The picture shows the K⁺ uptake through Na⁺,K⁺-ATPase and Na⁺-K⁺-2Cl⁻ cotransporter, K⁺ into cells against their concentration gradient; sources of Ca²⁺ are shown, including the voltage-dependent Ca²⁺ channel and Ca²⁺ release from sarcoplasmic reticulum (SR) mediated by a signal messenger (IP₃). When PE excites a vascular smooth muscle cell, there is stimulation of the alpha-adrenergic receptor leading to depolarization, resulting a status of vasoconstriction by increment of intracellular Ca²⁺ concentrations. Simultaneously, endothelial nitric oxide synthase (eNOS) stimulated by intracellular Ca²⁺ from vascular smooth muscle cell releases NO, and induces an increased K⁺ uptake via protein kinase G (PKG) to repolarize the vascular smooth muscle cell by opening K⁺ channels