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Several intracellular enzymes have been shown to have altered total activity or isoenzyme composition in cardiac hypertrophy. This study tests the hypothesis that the accumulation of the fetal-type (BB + MB) creatine kinase (CK) isoenzymes in hypertrophied adult myocardium is related to an increase in blood pressure. Consideration was made for the location, size, and hemodynamic load of the myocytes. By using the two-kidney, one-clip (2K1C) rat model of renal hypertension with and without hydralazine treatment, CK (total and isoenzyme), lactate dehydrogenase, and citrate synthase activities and myocyte size were measured. An increased heart weight/body weight ratio occurred in both untreated 2K1C rats (4.15 +/- 0.09) and hydralazine-treated 2K1C rats (4.12 +/- 0.13) as compared with control rats (3.25 +/- 0.10). Blood pressure was high only in untreated 2K1C rats (196 +/- 9 mm Hg), as compared with hydralazine-treated 2K1C rats (142 +/- 6 mm Hg) and control rats (135 +/- 3 mm Hg). Myocytes were isolated from five ventricular regions: left ventricular epicardial and endocardial free wall, left and right halves of the interventricular septum, and right ventricular free wall. Regional differences in normal and hypertrophied myocardium were demonstrated for morphological and biochemical parameters, with the greatest changes occurring in left ventricular endocardium. The shift in CK isoenzyme expression toward accumulating more BB + MB was greater in "hypertensive hypertrophy" (untreated 2K1C rats) than in "nonhypertensive hypertrophy" (hydralazine-treated 2K1C rats). Calculations incorporating isolated myocyte volume showed that the cellular content of total CK remained the same during the hypertrophic process, accounting for a decrease in the tissue activity. Measurement of lactate dehydrogenase and citrate synthase activities suggests that hypertrophied myocardium has relatively higher glycolytic capacity and that this effect is exacerbated in the presence of high blood pressure. We conclude that increased blood pressure is more closely linked to the fetal CK isoenzyme shift than is hypertrophy alone.
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
May 1988,
Journal of molecular and cellular cardiology,
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
December 1989,
Journal of hypertension. Supplement : official journal of the International Society of Hypertension,
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
July 1991,
Circulation research,
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
January 1979,
Hypertension (Dallas, Tex. : 1979),
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
January 1990,
Basic research in cardiology,
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
October 1985,
Journal of molecular and cellular cardiology,
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
May 2000,
American journal of physiology. Heart and circulatory physiology,
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
October 1994,
The American journal of physiology,
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
July 1991,
Circulation research,
S H Smith, and
M F Kramer, and
I Reis, and
S P Bishop, and
J S Ingwall
December 1987,
Laboratory investigation; a journal of technical methods and pathology,
