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. 2019 Nov 30;8(12):1551. doi: 10.3390/cells8121551

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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(A) Model of the role of angiotensin II (Ang II) AT1 and AT2 receptor activity on the proliferation of V-SVZ cells. Ang II, via AT1 receptors, set a basal inhibition of proliferation that was antagonized by the AT2 receptors, which set a basal level of Ang II-dependent regulation of neurogenesis. In addition, AT2 receptor activity may exert an additional direct stimulatory effect on proliferation, which was modulated by Mas receptors (MasR). (B) Aging, candesartan (or AT1 deletion), and PD (or AT2 deletion) regulate AT1/AT2 expression ratio. Aging and PD (or AT2 deletion) increased ratio and candesartan (or AT1 deletion) increased ratio in mice (i.e., decreased AT2 expression) and decreased ratio in rats (i.e., increased AT2 expression). Candesartan = AT1 receptor antagonist; PD123319 = AT2 receptor antagonist.