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Departments of Physiology and Biophysics, Morphology, Department of Biochemistry and Molecular Biology, Max‐Delbrück Center for Molecular Medicine (MDC), Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil
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Angiotensin (Ang)-(1–7) is now recognized as a biologically active component of the renin–angiotensin system (RAS). Ang-(1–7) appears to play a central role in the RAS because it exerts a vast array of actions, many of them opposite to those attributed to the main effector peptide of the RAS, Ang II. The discovery of the Ang-converting enzyme (ACE) homolog ACE2 brought to light an important metabolic pathway responsible for Ang-(1–7) synthesis. This enzyme can form Ang-(1–7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1–9) with subsequent Ang-(1–7) formation by ACE. In addition, it is now well established that the G protein-coupled receptor Mas is a functional binding site for Ang-(1–7). Thus, the axis formed by ACE2/Ang-(1–7)/Mas appears to represent an endogenous counterregulatory pathway within the RAS, the actions of which are in opposition to the vasoconstrictor/proliferative arm of the RAS consisting of ACE, Ang II, and AT1 receptor. In this brief review, we will discuss recent findings related to the biological role of the ACE2/Ang-(1–7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism. In addition, we will highlight the potential interactions of Ang-(1–7) and Mas with AT1 and AT2 receptors.
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SUMMARY
Estimations of human pituitary gonadotrophins (HPG), total 17-hydroxycorticosteroids, total 17-oxosteroids and oestrogens have been performed in seven hospitalized postmenopausal subjects receiving treatment with the dithiocarbamoylhydrazine derivatives Compound 22365 and Compound 33828 (Imperial Chemical Industries Ltd.).
Both compounds were shown to be inhibitors of pituitary gonadotrophic function as indicated by urinary HPG assays; Compound 33828 was more active in this respect than Compound 22365.
When Compound 22365 was administered to individual subjects at two different dose levels the time taken for urinary HPG levels to return to pretreatment values was longer in the case of the higher dose.
Neither of the compounds studied produced any effect on adrenocortical function as judged by urinary assays of 17-hydroxycorticosteroids, 17-oxosteroids and oestrogens.
Side effects were noted in two of the seven patients studied. In one subject with pre-existing liver damage it was necessary to stop treatment with Compound 22365 because of the development of mild jaundice.
