Cardiovascular structure and function after treatment with calcium entry inhibitors in hypertension

An intense research in the field of the structural cardiovascular alterations in experimental and clinical hypertension has carefully evaluated the heterogeneous nature and the clinical and physiopathological implications of either cardiac hypertrophy [1] or its vascular counterpart [2]. Thus, the importance of nonemodynamic factors in myocardial hypertrophy development, such as sympathetic stimuli [3, 4], has been elucidated even through the study of the effect of antihypertensive treatment [5, 6]. The lack of changes in myocardial mass during treatment with arteriolar vasodilators such as hydralazine or minoxidil was instrumental in developing that concept [6]. This chapter will focus on another group of vasodilators, the so called calcium entry blocker (CEB)s [7–23], rather recently brought to the front stage of antihypertensive treatment.