We postulate that the genetic factor increasing the propensity of black people of sub-Saharan African descent to develop high blood pressure is the relatively high activity of creatine kinase, predominantly in vascular and cardiac muscle tissue. Such greater activity of creatine kinase has been reported in skeletal muscle of black untrained subjects has been reported to be almost twice the activity found in white subjects. Creatine kinase, a key enzyme of cellular energy metabolism, increases the capacity of the cell 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 trans-membranous transport by readily providing the ATP needed for these processes. In addition, creatine kinase is increasingly reported to be involved in trophic responses. Furthermore, by using H+and ADP to synthesize ATP, creatine kinase prevents acidification of the cell, providing relative protection against the effects of ischaemia. 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 under chronic provocative circumstances, with higher mean blood pressures, more left ventricular hypertrophy and relatively fewer ischaemic events. Therefore, greater cellular activity of creatine kinase might explain the greater hypertension risk and the clinical characteristics of hypertensive disease observed in the black population.