BIOLOGICAL ADAPTATION AND DYSADAPTATION OF THE HEART TO CHRONIC ARTERIAL-HYPERTENSION - A REVIEW

Cardiac hypertrophy which occurs during chronic arterial hypertension is one of the numerous examples of biological adaptation to environmental requirements. As such, it is obtained at random by trial and error, and adaptation represents the sum of various modifications in gene expression, including the shift in isomyosin or in iso-Na+,K+-ATPase, the decrease in beta(1)-adrenergic or muscarinic receptors or in sarcoplasmic reticulum Ca2+-ATPase densities, and the unchanged density in calcium channels and current. Some of these changes are beneficial at the cellular level but are finally detrimental for the organism as a whole, such as slowing of maximum shortening velocity (V(max)). The prolonged calcium transient is likely to be a consequence of the various modifications of the membrane phenotype and provides a rational basis for arrhythmogenicity of the hypertrophied heart. There are also detrimental modifications, such as the increased collagen concentration and vascular hypertrophy, which may result from the accompanying changes in plasma content in several hormones or peptides.