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eNOS-derived NO induces relaxation of smooth muscle cells and, thus, increased dilation of all types of blood vessels, via a guanylyl cyclase-dependent mechanism.73 Lack of NO production by eNOS is believed to be a major causal factor in the development of vascular dysfunction and hypertension.74,75 eNOS, a highly regulated and complex enzyme, is inactive while bound to caveolin, and can be activated through calcium-responsive binding of calmodulin via hormonal or neuronal activation or shear stress-induced phosphorylation (Figure 1)

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Although some untreated TBI mice clearly had fields with large numbers of astrocytes, this was also the case for Sham controls and Immunocal®-pretreated mice subjected to TBI