The Epidemiology of Plasma Renin

Abstract

1. The epidemiological characteristics of plasma renin activity (PRA) were established in 1999 members of occupational groups in North and West London. 2. The main finding was that PRA was inversely associated with systolic blood pressure in men, the percentage fall in PRA (on a log scale) being 8.4% for each increase of one standard deviation in systolic blood pressure. There was a less obvious inverse relationship in women. 3. However, blood pressure accounted for less than 1% of the variance in PRA. 4. Mean PRA in both smokers and ex-smokers was about 20% higher than in non-smokers. 5. PRA fell with increasing age, was lower in women than in men and considerably lower in blacks (of either sex) than whites. 6. PRA was lower in the first quarter of the menstrual cycle than in the rest of the cycle. 7. Haemoglobin, blood cholesterol, leucocyte count and Factor VIII were positively correlated with PRA. 8. PRA was lower in men with diagnosed hypertension than in those without; there was no significant difference in the women. 9. PRA was lower in those who had had myocardial infarcts in the past than in those who had not. 10. The data as a whole suggest that it may be low, not high, levels of PRA which are associated with increased risks of cardiovascular disease in which hypertension is a predisposing factor. 11. The explanation may be a homoeostatic fall in PRA in response to a rise in blood pressure rather than a major causal role for PRA in the pathogenesis of essential hypertension and target-organ damage.

Why is plasma renin activity lower in populations of African origin?

“…Some of these studies spanning a period of nearly 25 years are summarised in Table 1. As can be seen, on average PRA in blacks is about 50% to that in whites and the differences are similar for men and women, 15,16 however it is also relevant to note the wide variability indicating that the PRA in a substantial proportion of blacks is likely to be in Values are means ± s.d. (n); PRA activity (ng/ml/hr); supine and for subjects on their normal sodium intake.…”

Angiotensin II–Induced Hypertension Accelerates the Development of Atherosclerosis in ApoE-Deficient Mice

“…Observational studies in humans have demonstrated that patients with high levels of circulating renin are at increased risk for myocardial infarction and other atherosclerotic cardiovascular events. 1,[22][23][24][25]32 In addition, studies in several different models of atherosclerosis have shown that ACE inhibitors and angiotensin-type 1 receptor antagonists inhibit atherosclerotic lesion formation. 18 -21 The mechanism whereby angiotensin II-induced hypertension accelerates and worsens atherosclerosis is probably multifactorial.…”

“…18 -21 Finally, numerous studies in humans have shown that high renin forms of hypertension are particularly proatherogenic and that patients with high renin hypertension are at increased risk of myocardial infarction. [22][23][24][25] The recently presented results of the Heart Outcomes Prevention Evaluation (HOPE) trial demonstrated a remarkable decrease in cardiovascular morbidity and mortality when normotensive individuals at increased risk for cardiovascular events were treated with an ACE inhibitor. 26 Taken together, these data specifically implicate the reninangiotensin II system in the pathogenesis of atherosclerosis.…”

Age and the pharmacodynamics of angiotensin converting enzyme inhibitors enalapril and enalaprilat.

“…The pharmacodynamic responses to these agents have been claimed to be directly related to plasma renin activity (Case et al, 1977), which falls with age (Meade et al, 1983 (Hockings et al, 1985). The pharmacokinetics of enalaprilat in these subjects is described in a separate paper (Hockings et al, 1986 Blood pressures and heart rate recordings were made at these times by means of a semi- Derkx et al, (1978).…”