| Abstract: | It is generally assumed that the beneficial effects of renin–angiotensin system blockers in cardiovascular disease are due to blockade of the generation or action of angiotensin at tissue sites. Such generation depends on the uptake of renin and/or its inactive precursor prorenin from the circulation. Recently, a (pro)renin receptor has been cloned that might perform this task. Unexpectedly, this receptor also induced angiotensin-independent effects, suggesting that renin and/or prorenin may act as agonists for this receptor. Ultimately, this could lead to the development of (pro)renin receptor blockers (i.e., drugs that not only prevent tissue angiotensin generation but also inhibit renin- or prorenin-induced effects). |
