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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 7. The molecular mechanism underlying selective activation of IK/SK channels in mesenteric arteries versus eNOS in pulmonary arteries.

Figure 7

In mesenteric arteries, Ca2+ entry through the TRPV4 channel at the myoendothelial projections (MEPs) determines vasodilation via activation of nearby small (SK) and intermediate (IK) conductance Ca2+-activated K+ channels. Co-localization of endothelial nitric oxide synthase (eNOS) with hemoglobin alpha (Hbα), a nitric oxide (NO) scavenging protein, prevents TRPV4-eNOS signaling. On the contrary, in pulmonary arteries, IK/SK channels and Hbα do not localize at MEPs. Therefore, Ca2+ influx via TRPV4 channel activates eNOS causing NO-dependent vasodilation. EC, endothelial cell.