Fig. 4.

Individual mean study values from hypertensive rat models showing the relationships between normalization of vascular superoxide (A) or normalization of kidney indices of ROS (B) and normalization of BP with prolonged tempol administration. The data were derived from the following animal models and studies: spontaneously hypertensive rats (SHR) (Fortepiani and Reckelhoff, 2005); Dahl salt-sensitive rats and fed salt rat (DSS + salt) (Meng et al., 2003; Nishiyama et al., 2004b); rats administrated deoxycorticosterone acetate, uninephrectomized, and fed salt (DOCA + salt): (Beswick et al., 2001; Nakano et al., 2003; Ghosh et al., 2004); rats infused with angiotensin II (Ang II) (Ortiz et al., 2001a; Hattori et al., 2005; Welch et al., 2005a); rats infused with aldosterone and fed salt (Aldo + salt) (Iglarz et al., 2004; Nishiyama et al., 2004a); rats transgenic for the human renin-2 gene (Ren-2) (Whaley-Connell et al., 2007); one kidney, one clip Goldblatt rat model of renovascular hypertension (IK,1C) (Dobrian et al., 2001; Christensen et al., 2007b); rats infused with endothelin-1 (ET models): (Sedeek et al., 2003; Elmarakby et al., 2005); and other hypertensive models: (Nishiyama et al., 2003; Banday et al., 2005; Stewart et al., 2005).