Table 1.
Cell type-specific regulation of vasodilation and vasoconstriction
| Vascular cell types | Vasodilation | Vasoconstriction |
|---|---|---|
| Vascular mural cells |
• Hyperpolarization: K+ channels ↑, Ca2+ channels ↓[55] • Activation of NO-cGMP-PKG pathway [63] • Activation of cAMP-PKA pathway [65] |
• Depolarization: K+ channels ↓, Ca2+ channels ↑[55] • Cytosolic Ca2+ increase mediated by IP3 receptor [56] • Activation of RhoA/Rho-kinase pathway [57] |
| Neurons |
• NMDA and AMPA glutamate receptor-dependent: ◦ NO release through nNOS [62] ◦ PGI2 synthesis [62] |
• NPY release from activated inhibitory neurons [66] • VP release from VP neurons in the SON [67] |
| Astrocytes |
• mGluR-dependent PGE2 and EET synthesis [60] • Astrocytic end feet K+ release in response to increased cytosolic Ca2+ [61] |
• Excess increase of cytosolic Ca2+ induced by Angiotensin II through AT1 receptor [68] |
| Endothelial cells |
• NO release through eNOS induced by: ◦ Glutamate signaling via NMDAR [69] ◦ Shear stress [70] |
• ET release induced by hypoxia, thrombin, and inflammatory cytokines [71] • ONOO− production by Angiotensin II through AT1-NOX pathway [72] |