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. Author manuscript; available in PMC: 2012 Feb 1.
Published in final edited form as: J Invest Dermatol. 2011 Apr 28;131(8):1754–1760. doi: 10.1038/jid.2011.96

Figure 6.

Figure 6

Schematic of hypothesized mechanism of vasoaction for purified curcumin I in the peripheral microcirculation for terminal (nutritive) arterioles or arcade arterioles that feed them. EC, endothelial cell; VSM, vascular smooth muscle cell; β-AD, beta adrenoceptor (EC or VSM dilation); α-AD, alpha adrenoceptor (VSM constriction). Curcumin induces vasoconstriction that requires α-AD, and vasodilation that requires β-AD. EC dependent dilation occurs through eNOS (endothelial nitric oxide synthase), NO (nitric oxide), and cGMP (cyclic guanosine monophosphate) accounts for most of the dilation; we hypothesize that this is linked to the receptor G-protein subunit, Gq and independent of Gi or MAPK (mitogen activating protein kinase) activity. VSM dependent dilation occurs through cAMP (cyclic adenosine monophosphate) accounts for a smaller portion of the dilation, significant in only the arcade arterioles; based on the data presented here, we hypothesize that this is linked to the G-protein subunit, Gαs.