The renin-angiotensin system (RAS) has long been recognized as an important regulator of blood pressure and electrolyte balance in mammals. The RAS exerts its effects through the generation and action of angiotensin II (Ang II), which has potent vasoconstrictor, antinatriuretic, and dipsogenic properties. Ang II is generated by the serial cleavage of angiotensinogen, first by the aspartyl protease renin, and then by the carboxydipeptidase angiotensin converting enzyme (ACE). Ang II acts as both an endocrine hormone and an autocrine and paracrine effector, notably in the kidney, heart, and brain, where it can be synthesized locally. Studies of gene-targeted mice reveal that in addition to having cardiovascular effects, the RAS is required during development, in particular during the postnatal period as development of the kidney continues (1).
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Curt D. Sigmund (2002) studied this question.
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