Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Regional changes in creatine kinase and myocyte size in hypertensive and nonhypertensive cardiac hypertrophy. 214 29

During myocardial hypertrophy, histological modifications induce a partial ischemic state and hemodynamic perturbations are responsible for an increased myocardial oxygen demand. The purpose of this study is to better characterize the alterations of intermediary metabolism linked to hemodynamic perturbations by carbon 13 NMR using enriched substrates. Left ventricular hypertrophy was consecutive to a renal hypertension (Goldblatt 2K-1C, 9 weeks). Myocardial compliance and contractility (left ventricular end diastolic pressure (LVEDP), +dP/dt max, +dP/dt max normalized to developed pressure (+dP/dt max/DEVP)) were estimated on Langendorff isolated perfused hearts at a constant perfusion pressure (normo and hypertensive rats (RHR)). Using (2-13C) acetate enriched (10 nm) substrate, 13C NMR spectra were obtained from tissue perchloric extracts. Mathematical model proposed by Malloy was used to analyze these 13C NMR spectra terms of metabolic fluxes: Fc2 = The fraction of (2-13C) acetyl-CoA entering the tricarboxylic acid cycle; y = The ratio between the activity of anaplerotic reactions to that of citrate synthetase. The results showed after hypoxia: an increase of LVEDP more pronounced in RHR (RHR: 48 +/- 15 mmHg VS SHAM: 22 +/- 6 mmHg, p < 0.01); a significant impairment of coronary blood flow more important in RHR; a significant increase of the ratio y in hypertrophied hearts (RHR: 0.062 +/- 0.09 VS SHAM: 0.15 +/- 0.02, p < 0.05). In conclusion, this study allowed a new approach to correlate diastolic dysfunction with metabolic data consecutive to an increased sensitiveness hypertrophy to hypoxic damages.
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PMID:[Metabolic aspects of hemodynamic behavior in left ventricular hypertrophy by 13C NMR]. 812 13