Abstract

This editorial refers to ‘Association of plasma renin with 10-year cardiovascular mortality, sudden cardiac death, and death due to heart failure’, by A. Tomaschitz et al. doi:10.1093/eurheartj/ehr150. Renin, the renal pressor substance, was discovered and described by Tigerstedt and Bergman in classic experiments published in 1898. It was not, however, until 1934 that Goldblatt identified the relevance of renin by showing that renal secretion of renin caused sustained renovascular hypertension in dogs. Others subsequently demonstrated that renin itself is not the pressor element, but rather is the rate-limiting component of the newly defined renin–angiotensin–aldosterone control system (RAAS).1 This RAAS has since become recognized as a key regulator of blood pressure control and a participating factor in its pathological consequences. In the past half century, the role of the RAAS in the pathophysiology of hypertension and as a basis for antihypertensive drug development was established.2,3 Plasma renin has also been associated with cardiovascular morbidity and mortality in hypertensive patients ( Figure 1 ).4,5 Tomaschitz et al. have now extended that finding to patients in whom plasma renin was measured while taking antihypertensive drugs.6 Figure 1 Adapted by permission from Macmillan Publishers Ltd: American Journal of Hypertension , Michael H. Alderman, Wee Lock Ooi, Hillel Cohen, Shantha Madhavan, Jean E. Sealey, John H. Laragh, Plasma renin activity: a risk factor for myocardial infarction in hypertensive patients, copyright (1997). Tomaschitz et al. measured the plasma renin concentration (PRC) using a sensitive automated immunoreactive chemiluminscence method that is comparable with the more traditional enzyme kinetic radioimmunoassay renin activity (PRA) assay. An exception is …

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