The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Angiotensin II type 2 receptor overexpression activates the vascular kinin system and causes vasodilation
Open accessAbstract
Angiotensin II (Ang II) is a potent vasopressor peptide that interacts with 2 major receptor isoforms - AT1 and AT2. Although blood pressure is increased in AT2 knockout mice, the underlying mechanisms remain undefined because of the low levels of expression of AT2 in the vasculature. Here we overexpressed AT2 in vascular smooth muscle (VSM) cells in transgenic (TG) mice. Aortic AT1 was not affected by overexpression of AT2. Chronic infusion of Ang II into AT2-TG mice completely abolished the AT1-mediated pressor effect, which was blocked by inhibitors of bradykinin type 2 receptor (icatibant) and nitric oxide (NO) synthase (L-NAME). Aortic explants from TG mice showed greatly increased cGMP production and diminished Ang II-induced vascular constriction. Removal of endothelium or treatment with icatibant and L-NAME abolished these AT2-mediated effects. AT2 blocked the amiloride-sensitive Na(+)/H(+) exchanger, promoting intracellular acidosis in VSM cells and activating kininogenases. The resulting enhancement of aortic kinin formation in TG mice was not affected by removal of endothelium. Our results suggest that AT2 in aortic VSM cells stimulates the production of bradykinin, which stimulates the NO/cGMP system in a paracrine manner to promote vasodilation. Selective stimulation of AT2 in the presence of AT1 antagonists is predicted to have a beneficial clinical effect in controlling blood pressure.
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Effects on blood pressure and exploratory behaviour of mice lacking angiotensin II type-2 receptor
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Behavioural and cardiovascular effects of disrupting the angiotensin II type-2 receptor gene in mice
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Cardiac Actions of Angiotensin II: Role of an Intracardiac Renin-Angiotensin System
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Pathophysiological Role of Angiotensin II Type 2 Receptor in Cardiovascular and Renal Diseases
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Cited by
Kamihata, H., Matsubara, H., Nishiue, T., Fujiyama, S., Tsutsumi, Y., Ozono, R., Masaki, H., Mori, Y., Iba, O., Tateishi, E., et al. (2001) · Circulation · doi:10.1161/hc3501.093817 · Cited by 965
Self-citationHypertension: Renin–Angiotensin–Aldosterone System Alterations
te Riet, L., van Esch, J. H. M., Roks, A. J. M., van den Meiracker, A. H., & Danser, A. H. J. (2015) · Circulation Research · doi:10.1161/circresaha.116.303587 · Cited by 706
Counter-regulatory renin–angiotensin system in cardiovascular disease
Paz Ocaranza, M., Riquelme, J. A., García, L., Jalil, J. E., Chiong, M., Santos, R. A. S., & Lavandero, S. (2020) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0244-8 · Cited by 561
Li, X. C., Zhang, J., & Zhuo, J. L. (2017) · Pharmacological Research · doi:10.1016/j.phrs.2017.06.005 · Cited by 435
Fujiyama, S., Amano, K., Uehira, K., Yoshida, M., Nishiwaki, Y., Nozawa, Y., Jin, D., Takai, S., Miyazaki, M., Egashira, K., et al. (2003) · Circulation Research · doi:10.1161/01.res.0000099245.08637.ce · Cited by 357
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Metadata
- Authors
- Tsutsumi, Y., Matsubara, H., Masaki, H., Kurihara, H., Murasawa, S., Takai, S., Miyazaki, M., Nozawa, Y., Ozono, R., Nakagawa, K., Miwa, T., Kawada, N., Mori, Y., Shibasaki, Y., Tanaka, Y., Fujiyama, S., Koyama, Y., Fujiyama, A., Takahashi, H., & Iwasaka, T.
- Venue
- Journal of Clinical Investigation
- Published
- 1999-10-01
- Volume
- 104
- Issue
- 7
- Pages
- 925-935
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2097489256
- Cited by
- 561
- References
- 38
- FWCI
- 28.29
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Tsutsumi, Y., Matsubara, H., Masaki, H., Kurihara, H., Murasawa, S., Takai, S., Miyazaki, M., Nozawa, Y., Ozono, R., Nakagawa, K., Miwa, T., Kawada, N., Mori, Y., Shibasaki, Y., Tanaka, Y., Fujiyama, S., Koyama, Y., Fujiyama, A., Takahashi, H., & Iwasaka, T. (1999). Angiotensin II type 2 receptor overexpression activates the vascular kinin system and causes vasodilation. Journal of Clinical Investigation. https://doi.org/10.1172/jci7886
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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