Myocardial fibrosis has drawn an attention as the pathogenesis of impaired diastolic function in hypertensive hearts. However, the mechanisms whereby hypertension provokes myocardial fibrosis are not fully understood. Recently, we have demonstrated that Wistar rat with a suprarenal aortic constriction is a model of cardiac hypertrophy associated with preserved systolic, but impaired diastolic function. In this model, a rapid blood pressure rise provokes transient upregulations of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant factor-1 (MCP-1) in the intramyocardial arteries, which in turn trigger perivascular macrophage infiltration. Following the inflammatory changes, myocardial fibrosis extends from perivascular to intermuscular interstitial spaces, which resulting in typical feature of reactive fibrosis. MCP-1 function blocking not only inhibits macrophage infiltration but also prevents reactive fibrosis and diastolic dysfunction, while not affecting blood pressure, myocyte hypertrophy, and systolic function. Tissue angiotensin system is a possible activator of perivascular inflammation. Accordingly, a substantial role of inflammation is suggested in myocardial fibrosis and diastolic dysfunction in hypertensive hearts. Targeting inflammation may be a new strategy for prevention and treatment of myocardial fibrosis and diastolic dysfunction in hypertensive hearts.