Another ace up the sleeve

摘要

It was only until recently that we thought the lung serves as an interface between air and blood where carbon dioxide is eliminated, oxygen is taken up and that is pretty much it. When in the early seventies reports came up that the lung converts angiotensin I (Ang I) to angioten-sin II (Ang II), we learned that it plays a role in the modulation of blood pressure and takes part in the renin-an-giotensin-aldosterone system (RAAS; fig. 1). The RAAS later proved to be much more complex than originally thought: the pulmonary vascular endothelium uses an-giotensin-converting enzyme 2 (ACE2) to degrade vaso-constrictive Ang II to Ang (1-7), a short-lived potent vasodilator in the pulmonary vascular bed [1, 2]. This in turn indicates that besides the well-known vasoconstric-tive leg, there is also a vasodilative leg of the RAAS (fig. 1) or, put differently, there is a flip-side to the known RAAS. During the past decade, a wealth of research on the biological functions of ACE2 has been performed and there have been some truly amazing findings. For instance, ACE2 may attenuate acute respiratory distress syndrome [2], and has proved to be responsible for cardiac contractility [3] as shown in rodent models. These two studies are of particular interest to the readership of this journal, as the respective authors demonstrate that ACE2 is involved in the regulation of the pulmonary arterial tone and is essential for heart function in vivo.