| Regional changes in creatine kinase and myocyte size in hypertensive and nonhypertensive cardiac hypertrophy. | |
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MedLine Citation:
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PMID: 2147129 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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S H Smith; M F Kramer; I Reis; S P Bishop; J S Ingwall |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Circulation research Volume: 67 ISSN: 0009-7330 ISO Abbreviation: Circ. Res. Publication Date: 1990 Dec |
Date Detail:
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Created Date: 1991-01-07 Completed Date: 1991-01-07 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1334-44 Citation Subset: IM |
Affiliation:
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Department of Pathology, University of Alabama, Birmingham 35294. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Biochemical Phenomena Biochemistry Blood Pressure Cardiomegaly / pathology* Citrate (si)-Synthase / analysis Creatine Kinase / analysis* Endocardium / enzymology, pathology Heart Atria / enzymology, pathology Heart Septum / enzymology, pathology Heart Ventricles / enzymology, pathology Hypertension / pathology* Hypertension, Renal / pathology Isoenzymes L-Lactate Dehydrogenase / analysis Male Myocardium / cytology, enzymology* Organ Size Rats Rats, Inbred Strains |
| Grant Support | |
ID/Acronym/Agency:
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2-K11-HL-01596/HL/NHLBI NIH HHS; HL-38189/HL/NHLBI NIH HHS; HL-43170/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Isoenzymes; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 2.3.3.1/Citrate (si)-Synthase; EC 2.7.3.2/Creatine Kinase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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