Blood Pressure, Resting Energy Expenditure, and Creatine Kinase Activity
To the Editor:
In a recent paper, Luke et al1 found a significant association between resting energy expenditure (REE) and blood pressure in black people of sub-Saharan African descent. This association was independent of the body mass index (BMI). The odds ratio for hypertension among participants in the highest versus lowest quartile of REE adjusted for body size and age was 1.7 (95% confidence interval, 1.1 to 2.7).
We read this paper with great interest, as the results presented are in-line with our postulate that a genetic factor that increases the ability of black people of sub-Saharan African descent to develop high blood pressures is relatively high activity of creatine kinase (CK), the central regulatory enzyme of cellular energy metabolism.2
Creatine kinase activity is reported to be a determinant of resting energy expenditure,3 and high activities of this enzyme are particularly described in black people.2 Creatine kinase increases the cell’s capacity to function under high demands. The enzyme regulates, buffers, and transports, via phosphocreatine and creatine, energy produced by glycolysis and oxidative phosphorylation to sites of energy consumption such as myofibrils and membrane ion pumps. At these cellular locations, it is involved in the contraction process and active transmembranous transport by readily providing ATP needed for these processes. Thus, greater creatine kinase activity in cardiovascular muscle and other tissues with high energy demands could increase cardiovascular contractile reserve, enhance trophic responses, and increase renal tubular ability to retain salt. This could facilitate the development of arterial hypertension.2,4 Therefore, individuals with higher physiological levels of creatine kinase activity might be more susceptible to develop chronic systemic arterial hypertension.2
In a recent random population sample of 1500 healthy black, white, and Asian people, systolic and diastolic blood pressure levels were respectively 9 and 5 mm Hg higher in those within the highest serum CK tertile at rest, as compared with those in the lowest CK tertile, when outcomes were corrected for BMI and age and other known causes of high serum CK were excluded.4 High serum CK activities and high blood pressure levels both occurred with greater frequency in black people in this study.4 Taken together, the results of Luke et al1 and our results4 both point to a possible role of the energy metabolism in the pathophysiology of hypertension. Those individuals with greater activity of cellular energy metabolism are proposed to have a greater energetic capacity to create and sustain high blood pressure levels.
Luke A,Adeyemo A,Kramer H,Forrester T,Cooper RS.Association between blood pressure and resting energy expenditure independent of body size.Hypertension. 2004;43:555–560.
Doucet E,Tremblay A,Simoneau JA,Joanisse DR.Skeletal muscle enzymes as predictors of 24-h energy metabolism in reduced-obese persons.Am J Clin Nutr. 2003;78:430–435.
Brewster LM,Mairuhu G,Stronks K,Bindraban N,Clark JF,van Montfrans GA.Serum creatine kinase as a marker of energetic capacity to create high blood pressure.J. Hypertens. 2003;21 (Suppl 4):S98.
Response: Blood Pressure, Resting Energy Expenditure, and Creatine Kinase Activity:
We appreciate the interest of Dr Brewster and Dr van Montfrans in our work on resting energy expenditure and blood pressure and are intrigued by the potential new insight suggested by their comments. Having reviewed the articles they cite in their letter to the editor, however, we are not as yet convinced that creatine kinase activity is an important determinant of energy expenditure measured at the whole-body level, but it clearly deserves further study.