Creatine kinase (CK) plays a central role in energy transfer in cells with high-energy demands, and the enzyme is rather susceptible to oxidative inactivation. The aim of the present study was to investigate whether the rate constant of forward CK reaction (kfor) is a suitable indicator of alterations in cerebral energy metabolism. We monitored kfor in the rat brain non-invasively by in vivo phosphorus (31P) magnetic resonance spectroscopy. To alter energy metabolism, we applied the following experimental models. Spontaneously hypertensive rats (SHR) were used as a model of moderate hypertension. To simulate severe hypertension, we kept SHR on 1% NaCl diet. To model cerebral insufficiency, we applied chronic cerebral hypoperfusion, performed by permanent occlusion of three out of four brain supplying vessels, in adult and aged rats (6 and 15 months old, respectively). No significant changes in kfor value were found in rats with moderate hypertension (SHR). However, we observed a significant decrease in k for in the brains of both adult and aged rats with severe hypertension. The most pronounced decrease in kfor was found in the brains under chronic hypoperfusion. In conclusion, the significant decrease of CK activity, found in severe hypertension and chronic hypoperfusion, may suggest that alterations of cerebral energy metabolism underlie cognitive impairments occurring in both pathological conditions.
|Original language||English (US)|
|Number of pages||4|
|Journal||Biologia - Section Cellular and Molecular Biology|
|Issue number||SUPPL. 17|
|State||Published - Dec 1 2005|
- Creatine kinase kinetics
- P MRS