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. Author manuscript; available in PMC: 2013 Apr 24.
Published in final edited form as: Crit Rev Biomed Eng. 2012;40(4):265–278. doi: 10.1615/critrevbiomedeng.v40.i4.30

FIGURE 3.

FIGURE 3

Putative molecular mechanisms by which CIH induces changes in vascular tone, resulting in the development of hypertension; “?” is used to designate hypothesized mechanism that has not been proven yet. Angiotensin II, ET1 and nNOS also play a role in CIH induced vascular changes resulting in hypertension. NFATc3, a nuclear factor involved in maintenance of vascular smooth muscle reactivity appears to be downstream of ET1 and appears to be important in the vascular changes and hypertension induced by CIH. (AT1—angiotensinII type 1 receptor; NOX—NADPH oxidase; ROS—reactive oxygen species; ET-1—endothelin 1; ETA—endothelin A receptor; nNOS— neuronal nitric oxide synthase; NFATc3—nuclear activator of T cells).