Key result
This review highlights recent advances in the biology of hypertensive cardiopathy, focusing on permanent myocyte changes including myosin kinetics, NO synthases, and apoptosis.
This review outlines the molecular and cellular adaptations of myocytes in hypertensive cardiopathy, providing insights into the biological basis of myocardial dysfunction.
May guide mechanistic research in hypertensive heart disease; leaves open clinical translation.
Available data suggest that hypertensive cardiopathy is principally determined by the phenoconversion that allows the myocyte to adapt to the new working conditions by re-expressing a fetal program. Nevertheless, in clinical conditions, the scheme is different. The above phenotype is modified by trophic factors, which originate from ischemia, senescence, diabetes, genetics, or neurohormonal reactions. This review only focuses on some of the most recent advances concerning the permanent changes in the myocyte. Changes in extracellular matrix have been excluded. Recently, emphasis has been on the kinetic basis of the myocardial dysfunction at the myosin level, the potential therapeutic utilization of transferring the adrenergic receptor gene, the participation of NO synthases in the adaptational process, the existence of an abnormal excitation-contraction coupling due to a redistribution of Ca2+ sparks, the role of the microtubule as a determinant of sarcomere motion, and the multifactorial origin of cell death by apoptosis.
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Swynghedauw et al. (2000) conducted a review in hypertensive cardiopathy. This review highlights recent advances in the biology of hypertensive cardiopathy, focusing on permanent myocyte changes including myosin kinetics, NO synthases, and apoptosis.