Early-stage 2K1C renovascular hypertension does not increase global MHC-II or F4/80 abundance in the non-clipped kidney but reveals focal F4/80+ induction.

The two-kidney, one-clip (2K1C) model produces renovascular hypertension. The effects on the clipped kidney (CK) are well described, while the non-clipped kidney (NCK) is used as a model to evaluate the effects of high blood pressure. Although most of these effects have been described at later stages of 2K1C hypertension, it remains unclear whether immune antigen-presenting cells (APCs) expand early in the NCK during the first stages of 2K1C hypertension. Our objective was to determine whether the 2K1C model increases the presence and/or distribution of APCs in the NCK during the early phase of renovascular hypertension. Male C57BL/6J mice underwent sham surgery or 2K1C surgery (n = 6). Blood pressure was assessed, and NCKs were collected on day 7. Global expression of major histocompatibility complex (MHC)-II (APC marker) and F4/80 (monocyte/macrophage lineage) was quantified by immunoblotting, while spatial distribution was evaluated by immunohistochemistry (IHC) and morphological analysis. 2K1C produced a significant increase in blood pressure in the NCK without albuminuria. Immunoblot experiments showed no significant differences in global MHC-II or F4/80 levels between sham and 2K1C groups in the NCK. However, IHC revealed a focal increase in F4/80+ signal and a significant rise in F4/80+ area fraction, consistent with localized monocytic/macrophage enrichment not captured by whole-tissue homogenates from NCK. By contrast, F4/80 immunostaining was observed in conspicuous resident cells. After 7 days of 2K1C hypertension, contralateral renal APC expansion is not evident at the global protein level, yet focal F4/80+ enrichment suggests early regional and focal immune remodelling that may precede later overt inflammation.