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. Author manuscript; available in PMC: 2023 Jul 31.
Published in final edited form as: Compr Physiol. 2021 Apr 1;11(2):1831–1869. doi: 10.1002/cphy.c200030

Figure 6. Signaling mechanisms at myoendothelial projections (MEPs) that control the communication between endothelial cells (ECs) and smooth muscle cells (SMCs) and SMC contractility.

Figure 6

Stimulation of Gq-protein coupled receptors (GqPCRs) on SMC membrane leads to the formation of inositol triphosphate (IP3) and diacylglycerol (DAG). DAG activates protein kinase C (PKC), which phosphorylates voltage-gated Ca2+ (CaV1.2) channel, leading to an increase in SMC Ca2+ and vasoconstriction. IP3 and Ca2+ can diffuse to ECs through myoendothelial gap junctions (MEGJ). Elevation of IP3 and Ca2+ at MEPs limits vasoconstriction by activating TRPV4-IK/SK channel and IP3R-IK/SK channel signaling. TRPV4, transient receptor potential vanilloid channel 4 (TRPV4); SK and IK, small (SK) and intermediate (IK) conductance Ca2+-activated K+ channels.