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.