In arterial hypertension, cardiac remodeling comprises myocyte hypertrophy, interstitial fibrosis, and functional and structural alterations of the coronary microcirculation. This leads to diastolic and systolic dysfunction of the left ventricle and impairment of coronary flow reserve. Consequently, antihypertensive treatment should aim at repairing hypertensive cardiac remodeling through reversing myocyte hypertrophy, restoring myocardial structure, and improving coronary flow reserve along with blood pressure normalization. Although it has been shown that regression of left ventricular hypertrophy (LVH) can be achieved by suitable antihypertensive therapy, more insight regarding the ability to repair coronary microcirculation is needed. In spontaneously hypertensive rats (SHRs), it has been shown that coronary reserve was enhanced after hydralazine administration without concomitant regression of LVH. Likewise, administration of the calcium-channel blocker felodipine led to a reversal of medial hypertrophy in coronary resistance vessels. The angiotensin-converting enzyme inhibitor lisinopril was shown to improve coronary reserve and to reverse both medial hypertrophy and myocardial fibrosis in SHRs. Increase in length density of capillaries with either nifedipine or moxonidine treatment was also found in experimental hypertension. First clinical data indicate that, after prolonged antihypertensive treatment, coronary flow reserve can be improved in hypertensive patients with microvascular disease. Further studies are warranted to elucidate whether improved coronary flow reserve after medical treatment for arterial hypertension is due to an influence of myocardial factors, such as LVH or myocardial fibrosis or to repair of the structurally remodeled microcirculation.