Evidence Supporting the Hypothesis That Inflammation-Induced Vasospasm Is Involved in the Pathogenesis of Acquired Sensorineural Hearing Loss

Figure 2

Mechanism of action of interleukin-1 (IL-1) via G-protein coupled receptors (GPCR) on reduction of nitric oxide (NO) production by reducing nitric oxide synthase (NOS) activity in the vascular endothelial cell (EC) and by activation of the enzyme Rho kinase via RhoA in the vascular smooth muscle cell to activate by phosphorylation through protein kinase C (PKC) myosine phosphatase targeting subunit-1 (MYPT1), protein kinase C-potentiated phosphatase inhibitor-17 (CPI-17 and myosine binding subunit (MBS)), which all three inhibit the myosine light chain phosphatase (MLCP) which dephosphorylates the myosine light chain, a process, which is necessary for smooth muscle relaxation. This process thus causes vasoconstriction.