Hypertrophy, after compensatory

It thus appears that the tissues of an organ such as the kidney secrete into the body substances which inhibit kidney tissue development, and that compensatory hypertrophy after kidney removal may be ascribed to a shortage of these inhibitors. On this view the relative size of each organ must be dictated by the concentration within the body space of... 

As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms (1) tachycardia and increased contractility through sympathetic nervous system activation (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume (3) vasoconstriction and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression. 

K43 Kolia, V. E., Bilich, G. L., Porollo, V. I., Otmakhov, V. N. and Suslova, O. I. Effect of potassium orotate on compensatory hypertrophy of the remaining lung after left-sided pulmonectomy. Eksp. Khir. Anesteziol., 4, 35-38 (1975) (Russ.)... 

Some of the metabolic changes in the kidney in such experiments are known. Sodium is temporarily depleted, and then ammonium excretion is markedly increased. The increased excretion of ammonium ions is accompanied by de novo synthesis of glutaminase. Although the adaptation just described can be expected, other metabolic changes observed in the kidney of animals made acidotic experimentally are somewhat more difficult to understand. They include increased activity of the enzymes of the hexose monophosphate shunt, increased rates of gluconeogenesis and lipogenesis, and compensatory hypertrophy of the kidney, somewhat reminiscent of that observed after unilateral nephrectomy [48]. 

Peltola [495] reported that large repeated doses of cortisone inhibits the thyroxine potentiation of the anaphylactoid reaction. Spencer and West [579, 580] then presented evidence that the action of the thyroid hormone is mediated through a temporary adrenocortical deficiency. These workers found that maximum sensitivity occurred only after prolonged treatment with the thyroid hormone, after which a return to normal in association with a compensatory adrenal hypertrophy occurred. On the other hand, hypothyroidism caused a temporary excess of the adrenal cortical hormones in the tissues followed by a homeostatic adrenal atrophy. 

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