MITOCHONDRIAL ENERGY-METABOLISM IN THE LEFT-VENTRICULAR TISSUE OF SPONTANEOUSLY HYPERTENSIVE RATS - ABNORMALITIES IN BOTH ADENINENUCLEOTIDEAND PHOSPHATE TRANSLOCATORS AND ENZYME ADENYLATE-KINASE AND CREATINE-PHOSPHOKINASE ACTIVITIES

Citation
Tm. Seccia et al., MITOCHONDRIAL ENERGY-METABOLISM IN THE LEFT-VENTRICULAR TISSUE OF SPONTANEOUSLY HYPERTENSIVE RATS - ABNORMALITIES IN BOTH ADENINENUCLEOTIDEAND PHOSPHATE TRANSLOCATORS AND ENZYME ADENYLATE-KINASE AND CREATINE-PHOSPHOKINASE ACTIVITIES, Clinical and experimental hypertension, 20(3), 1998, pp. 345-358
Citations number
40
Categorie Soggetti
Pharmacology & Pharmacy","Peripheal Vascular Diseas
ISSN journal
10641963
Volume
20
Issue
3
Year of publication
1998
Pages
345 - 358
Database
ISI
SICI code
1064-1963(1998)20:3<345:MEITLT>2.0.ZU;2-G
Abstract
The aim of this study was to investigate the oxidative phosphorylation and additional adenosinetriphosphate (ATP) production mechanisms in m itochondria isolated from hypertrophied left ventricles of spontaneous ly hypertensive rats (SHR). Measurements of adenosinediphosphate (ADP) /ATP and inorganic phosphate (Pi) carrier activities showed a signific ant reduction of Vmax values thus suggesting a general decrease of ATP supply in the hypertrophied ventricles. Investigation of mitochondria l enzyme activities showed 45% and 90% increases of adenylate-kinase a nd 80% and 110% increases of creatine-phosphokinase in 5- and 24-week- old SHR, before and after the development of the hypertensive state, r espectively. The abnormalities found in SHR at the mitochondrial level suggest a profound rearrangement of energy production mechanisms in t his model of left ventricular hypertrophy; whether the defects are det ermined genetically, and then worsen with the hypertensive state, rema ins to be determined.