Biochemical aspects of experimental cardiac hypertrophy.
In experimental cardiac hypertrophy induced by aortic constriction of rats, the hypertrophy was established after 5-7 days. The basic biochemical changes for increasing tissue mass; increases in protein, nucleic acid, and polyamine synthesis started to occur between 2 and 8 hours followed by an increase in uridine nucleotide pools via predominance of "salvage" pathway. Although the precise coupling mechanism between mechanical stress and biochemical changes is still obscure, an interval between increased load and DNA transcription may be quite short. Some of the key enzymes regulating these processes showed a biphasic response the reason of which is not clear. The established hypertrophied heart muscle showed a decrease in velocity of isotonic shortening and an increase in resting tension. The former alteration is referred to a decrease in myosin ATPase activity and an disorder in excitation-contraction coupling mechanism, and the latter is supposed to be due to an increase in collagen in heart muscle.
D000251:Adenosine Triphosphatases / Q000096:biosynthesis; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism* / Q000503:physiopathology; D004247:DNA / Q000096:biosynthesis; D004195:Disease Models, Animal; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000096:biosynthesis; D011700:Putrescine / Q000096:biosynthesis; D011742:Pyrimidine Nucleotides / Q000096:biosynthesis; D012313:RNA / Q000096:biosynthesis; D051381:Rats; D013095:Spermidine / Q000096:biosynthesis; D013096:Spermine / Q000096:biosynthesis
D011742:Pyrimidine Nucleotides; D013096:Spermine; D012313:RNA; D004247:DNA; D000251:Adenosine Triphosphatases; D009218:Myosins; D013095:Spermidine; D011700:Putrescine