Hypertension is a major driver of cardiovascular and renal injury and is increasingly recognized as a chronic inflammatory disorder rather than solely a hemodynamic disease. Persistent elevation of blood pressure promotes activation of the renin–angiotensin–aldosterone system (RAAS), sympathetic nervous system, oxidative stress, endothelial dysfunction, immune-cell activation, and maladaptive extracellular-matrix remodeling. These processes interact bidirectionally between the heart and kidneys, creating a self-reinforcing cardiorenal inflammatory–fibrotic cycle. Angiotensin II and aldosterone stimulate reactive oxygen species production, inflammatory signaling, and profibrotic pathways, including transforming growth factor-β (TGF-β)/Smad and connective tissue growth factor pathways. In parallel, activation of macrophages, T cells, monocytes, and inflammasome pathways promotes the release of cytokines such as tumour necrosis factor-α, interleukin-1β, and interleukin-6. Chronic inflammation subsequently activates fibroblasts and myofibroblasts, leading to excessive deposition of extracellular-matrix proteins and progressive fibrosis in the myocardium and kidney. Cardiac fibrosis contributes to ventricular stiffness, hypertrophy, and impaired function, whereas renal glomerular and tubulointerstitial fibrosis progressively reduces filtration capacity. The resulting decline in renal function further aggravates cardiovascular stress through volume overload, neurohormonal activation, and systemic inflammation. Understanding this interconnected inflammation–oxidative stress–fibrosis network provides an important framework for developing therapies aimed not only at lowering blood pressure but also at preventing or reversing target-organ damage.