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Table 1 Cell type-specific regulation of vasodilation and vasoconstriction

From: Pathophysiology and probable etiology of cerebral small vessel disease in vascular dementia and Alzheimer’s disease

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]