Abstract
Angiotensin (Ang) II is pro‐inflammatory, and T cells contribute to Ang II hypertension in male animal models; little is known in females. Initial studies treated 12 wk old male and female Sprague Dawley rats (SD) with Ang II (200 ng/kg/min) and renal T cell profiles were measured via flow cytometry. Ang II increased renal T cell infiltration in both sexes; as well as immuno‐suppressive T regulatory cells (Tregs) only in kidneys of female SD (p=0.004), and male SD had greater increases in pro‐inflammatory Th17 cells (p<0.001). We have previously shown that females also have greater renal Ang (1‐7) levels than males, and Ang (1‐7) has been suggested to be anti‐inflammatory. Therefore, the goal of the current study was to test the hypothesis that chronic Ang II infusion increases renal T cells in both sexes; however, greater Ang (1‐7) results in more Tregs in females than males. Additional male and female SD were treated with Ang II, or Ang II plus the Ang (1‐7) mas receptor antagonist A‐779 (48 µg/kg/hr). CD4+ T cell counts were greater in males compared to females following Ang II infusion (p<0.01), inhibition of Ang (1‐7) did not alter counts in either sex. Ang II infusion increased Tregs in females and Th17 in males, inhibition of Ang (1‐7) did not alter these counts. Renal CD8+ T cell counts were reduced in males relative to females following Ang II infusion (p<0.01), and inhibition of Ang (1‐7) caused a significant but comparable decrease in renal CD8+ T cell counts in both sexes (p=0.0003). In conclusion, our data implicates a role for Ang (1‐7) to modulate Ang II‐induced changes in CD8+ T cell counts; however, our results show that Ang (1‐7) does not mediate the sex difference in Tregs and Th17 in SD during Ang II infusion.Grant Funding Source: Supported by NIH grant 1R01 HL093271‐01A1 to J.C.S, and AHA Predoctoral Fellowship 12PRE11470003 to M.A.Z.
Published Version
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