Abstract 246: Interleukin-1 Potentiates Renal Sodium Retention in Angiotensin Ii-dependent Hypertension by Preventing No-mediated Inhibition of the Na+-k+-2cl- Cotransporter

The current studies define the mechanism through which interleukin-1 receptor (IL-1R) activation exacerbates angiotensin (Ang) II-induced hypertension. We previously reported that IL-1R-deficient (KO) mice had attenuated elevations in blood pressure (BP) vs. wild-types (WT) in our hypertension model of uni-nephrectomy followed by 4 wks of Ang II infusion. As the IL-1 receptor modulates macrophage function, we blindly counted F4/80+ macrophages in KO and WT kidneys after 4 wks of Ang II. Compared to WTs, the KO kidneys contained more macrophages (13.6±1.7 vs. 17.9±0.8 per HPF; p=0.03) and had higher mRNA levels of the macrophage cytokine iNOS (1.0±0.2 vs. 1.7±0.3 au; p