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K<jats:sub>V<\/jats:sub>1.3 channels are also expressed in macrophages, where they assemble with K<jats:sub>V<\/jats:sub>1.5 channels (K<jats:sub>V<\/jats:sub>1.3\/K<jats:sub>V<\/jats:sub>1.5), whose activation generates a K<jats:sub>V<\/jats:sub> current. In macrophages, the K<jats:sub>V<\/jats:sub>1.3\/K<jats:sub>V<\/jats:sub>1.5 ratio is increased by classical activation (M1). Whether these channels are involved in angiotensin II (AngII)\u2010induced vascular remodelling, and whether they can modulate the macrophage phenotype in hypertension, remains unknown. We characterized the role of K<jats:sub>V<\/jats:sub>1.3 channels in vascular damage in hypertension.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p>We used AngII\u2010infused mice treated with two selective K<jats:sub>V<\/jats:sub>1.3 channel inhibitors (HsTX[R14A] and [EWSS]ShK). Vascular function and structure were measured using wire and pressure myography, respectively. VSMC and macrophage electrophysiology were studied using the patch\u2010clamp technique; gene expression was analysed using RT\u2010PCR.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>AngII increased K<jats:sub>V<\/jats:sub>1.3 channel expression in mice aorta and peritoneal macrophages which was abolished by HsTX[R14A] treatment. K<jats:sub>V<\/jats:sub>1.3 inhibition did not prevent hypertension, vascular remodelling, or stiffness but corrected AngII\u2010induced macrophage infiltration and endothelial dysfunction in the small mesenteric arteries and\/or aorta, via a mechanism independent of electrophysiological changes in VSMCs. AngII modified the electrophysiological properties of peritoneal macrophages, indicating an M1\u2010like activated state, with enhanced expression of proinflammatory cytokines that induced endothelial dysfunction. 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