1986), African Americans (He et al., 1998; Weinberger, 1993; Weinberger et al., 1986), and older individuals, both nonhypertensive and hypertensive (Weinberger and Fineberg, 1991). In one prospective observational study, an elevated renin/sodium profile (plasma renin activity of 7.1 ng/mL/hour and urinary sodium excretion of 100 mmol/day or plasma renin activity of 5 ng/mL/hour and 200 mmol/day) was associated with a significantly higher risk for myocardial infarction in hypertensive men (Alderman et al., 1991). However, the number of events was small, just 27, and no other study has replicated these findings. In contrast, in another study of primarily nonhypertensive individuals (Meade et al., 1993), no relationship was found between plasma renin activity and the incidence of myocardial infarction or sudden death from coronary causes. In this study, there were 86 ischemic heart disease events.
Plasma renin activity has also been reported to be associated with left ventricular hypertrophy and insulin resistance (Aronow et al., 1997; Koga et al., 1998, Townsend and Zhao, 1994). A high renin profile has been associated with other cardiovascular risk factors, including elevated plasma cholesterol and triglyceride concentrations and lower high-density lipoprotein concentrations (Allikmets et al., 1996).
The clinical relevance of a rise in plasma renin activity in response to blood pressure reduction is uncertain. Plasma renin activity commonly rises in response to therapies that lower blood pressure and cardiovascular disease risk. For example, thiazide diuretic therapy commonly leads to a rise in plasma renin activity (Niarchos et al., 1984). Yet despite this rise, diuretic therapy has been repeatedly shown to prevent stroke and coronary heart disease (Psaty et al., 2003). In a meta-analysis of 42 trials that compared the effects of seven different classes of antihypertensive medications, the net effects on coronary heart disease of low-dose thiazide diuretics (which raise plasma renin activity) and angiotensin converting enzyme inhibitors (which lower plasma renin activity) were identical (relative risk of 1.0).
Some investigators have interpreted the rise in plasma renin activity from a reduced sodium intake as a deleterious response that mitigates the potential benefits of sodium reduction on blood pressure (Alderman et al., 1991). While this concern is theoretically plausible, there is insufficient evidence in support of this claim. Furthermore, in contrast to blood pressure, which is a well-accepted cardiovascular risk factor, there is no such consensus on the interpretation of plasma renin activity and its role in guiding nonpharmacological or pharmacological therapy for high blood pressure.