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This Article Full Text Full Text (PDF) All Versions of this Article: 93/5/528    most recent expphysiol.2007.040345v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Alenina, N. Articles by Bader, M. Search for Related Content PubMed PubMed Citation Articles by Alenina, N. Articles by Bader, M. Related Collections Review Articles Vascular

¹ Max-Delbrück-Center for Molecular Medicine (MDC), D-13092 Berlin-Buch, Germany ² Institute for Experimental Medicine, Russian Academy of Medical Sciences, St Petersburg, Russia

Mas is the receptor for angiotensin-(1–7) and is involved in cardiovascular and neuronal regulation, in which the heptapeptide also plays a major role. Mas-deficient mice have been generated by us, and their characterization has shown that Mas has important functions in behaviour and cardiovascular regulation. These mice exhibit increased anxiety but, despite an enhanced long-term potentiation in the hippocampus, do not perform better in learning experiments. When Mas-deficient mice are backcrossed to the FVB/N genetic background, a cardiovascular phenotype is uncovered, in that the backcrossed animals become hypertensive. Concordant with our detection by fluorescent in situ hybridization of Mas mRNA in mouse endothelium, this phenotype is caused by endothelial dysfunction based on a dysbalance between nitric oxide and reactive oxygen species in the vessel wall. In agreement with these data, transgenic spontaneously hypertensive stroke-prone rats overexpressing ACE2 in the vessel wall exhibit reduced blood pressure as a result of improved endothelial function. Moreover, angiotensin-(1–7) overexpression in transgenic rats has cardioprotective and haemodynamic effects. In conclusion, the angiotensin-(1–7)–Mas axis has important functional implications for vascular regulation and blood pressure control, particularly in pathophysiological situations.

(Received 15 November 2007; accepted after revision 17 December 2007; first published online 21 December 2007)
Corresponding author M. Bader: Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Strasse 10, D-13092 Berlin-Buch, Germany. Email: mbader{at}mdc-berlin.de