The HMGB1 increase was proportionately and relatively greater in LA than in RA, the same holds true for the NFkB activation, inflammatory infiltrates and IL-6 production, so that one can postulate that although some changes such as RAGE/sRAGE regulation may not in principle be blood pressure dependent, hypertension directly or indirectly potentiates the changes, possibly due to the increase in AGEs such as CML in the left atrium, which in turn would potentiate RAGE expression. Here, NFKB1 is linked to hypertensive disorder.