Chronic hypertension and diabetes produce both macrovascular and microvascular pathophysiological changes. Greater arterial stiffness increases central systolic and pulse pressure, which raises left ventricular afterload and reduces coronary perfusion. Resistance arteries remodelling and capillary rarefaction increase peripheral resistance, thereby contributing to hypertension and amplifying the detrimental haemodynamic effects of arterial stiffening. The result is target organ impairment, such as left ventricular hypertrophy, decreased coronary perfusion pressure, reduced coronary reserve and further vascular remodelling, culminating in coronary artery disease and stroke. Therapeutic intervention is possible and necessary to stop these vascular changes. Vasodilating antihypertensive drugs, such as the perindopril/indapamide combination, have been shown to modify both arterial and arteriolar remodelling, leading to reduced central systolic blood pressure and enhancing vascular bed perfusion. These effects probably underpin the benefits of these agents in reducing cardiovascular morbidity and mortality.