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Highlights the potential role of aldosterone synthase (CYP11B2) genetic linkage in blood pressure response to exercise and the broader pathogenesis of hypertension.
In Rankinen and colleagues' report, 1 the strongest genetic linkage in the whole study was found in chromosome 8q21 (Lod 2.36, P0.0005) for the effect of exercise training on submaximal exercise systolic blood pressure (BP) response during cycle ergometry at 50 watts. This locus incidentally contains the gene for CYP11B2 that codes for aldosterone synthase, a key rate-limiting enzyme for the biosynthesis of aldosterone. This is an important finding, albeit limited to the sedentary white population with normal resting BP. The role of aldosterone in the pathogenesis of hypertension is gaining wider recognition with the finding that nearly 1 in 10 hypertensives has inappropriate aldosterone activity that is amenable to treatment. 2 A recent study found a significant association between submaximal exercise systolic BP and the aldosterone-to-renin ratio, a marker of inappropriate aldosterone activity within the hypertensive population. 3 Another related study found a significant relationship between aldosterone synthase polymorphism and inappropriate aldosterone activity, and this relationship appeared to strengthen with age. 4 What, then, is the clinical significance of Rankinen and colleagues' findings?
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Pitt Lim (2002) studied this question.
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