The changes in ventricular isomyosin composition and Ca2+-activated ATPase activity occurring with regression of both hypertension and cardiac hypertrophy were investigated by using polyacrylamide gel electrophoresis under nondenaturing conditions, heavy chain peptide mapping, and an enzymatic assay. Eight control male Wistar rats and 14 two-kidney, one clip (Goldblatt II) hypertensive rats were studied from the fifth week of age. At 10 weeks of age, five Goldblatt II rats and four normotensive controls were killed. Five other Goldblatt II rats underwent nephrectomy of the ischemic kidney, which resulted in subsequent normalization of blood pressure. The remaining four control, four Goldblatt II rats, and five nephrectomized rats were killed at 15 weeks of age. Both the 10- and 15-week-old hypertensive rats had a significantly higher (p-2 vs 2.75 ± 0.25 x 10-2; 5.93 ± 2.26 x 10-2 vs 2.65 ± 0.17 x 10-2). The 15-week-old nephrectomized rats had a biventricular weight to body weight ratio (2.90 ± 0.25 x 10-2) close to that of age-matched controls and significantly lower (p2+-activated ATPase was significantly lower (p2 and V3 was evident in the hypertensive animals, which displayed a decrease of the 'fast' V1 isoenzyme. Through peptide mapping of myosin heavy chains, an additional band was found in both groups of hypertensive animals that was absent in the age-matched controls. Nephrectomized 15-week-old rats showed a ventricular isomyosin composition and peptide mapping similar to that of age-matched controls. In conclusion, with normalization of blood pressure, complete reversal of cardiac hypertrophy was achieved and the biochemical and molecular properties of left ventricular myosin were fully restored.
|Number of pages||6|
|Publication status||Published - 1986|
ASJC Scopus subject areas
- Internal Medicine