Collagen metabolism in experimental cardiac hypertrophy in the rat and the effect of digitoxin treatment.
It is generally agreed that cardiac hypertrophy is accompanied by the hyperplasia of connective tissue cells. In the present work, collagen metabolism was studied in the heart of nondigitalised and digitalised rats after the constriction of the aorta. The activity of prolyl hydroxylase was maximally increased 2 days after the operation. The incorporation of proline into collagen hydroxyproline increased without any increase in the specific radioactivity of free intracellular proline, the peak labelling of collagen occurring at 4 days. Although the treatment of the rats with digitoxin prevented the development of cardiac hypertrophy and an increase in collagen labelling, an increase in the activity of prolyl hydroxylase was observed. The intracellular free proline pool and its specific radioactivity were significantly lower in digitalised rats as compared with non-digitalised rats. The results indicate that constriction of the aorta is accompanied by an activation of connective tissue cells leading to increased synthesis of collagen. However, digitoxin treatment can prevent the increase in collagen labelling, possibly by inhibiting the amino acid transport, but it is unable to remove the stimulus for hypertrophy.
D000621:Aminoisobutyric Acids / Q000378:metabolism; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism* / Q000517:prevention & control; D003094:Collagen / Q000096:biosynthesis*; D004074:Digitoxin / Q000008:administration & dosage*; D005110:Extracellular Space; D006321:Heart / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000201:enzymology; D011393:Procollagen-Proline Dioxygenase / Q000378:metabolism; D011392:Proline / Q000378:metabolism; D051381:Rats
D000621:Aminoisobutyric Acids; D003094:Collagen; D011392:Proline; D004074:Digitoxin; D011393:Procollagen-Proline Dioxygenase