AT1-receptor heterodimers show enhanced G-protein activation and altered receptor sequestration

Said AbdAlla, Heinz Lother and Ursula Quitterer ()
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Said AbdAlla: Genetics Engineering and Biotechnology Research Institute
Heinz Lother: Heinrich Pette Institut
Ursula Quitterer: Institut für Pharmakologie

Nature, 2000, vol. 407, issue 6800, 94-98

Abstract: Abstract The vasopressor angiotensin II regulates vascular contractility and blood pressure through binding to type 1 angiotensin II receptors (AT1; refs 1, 2). Bradykinin, a vasodepressor, is a functional antagonist of angiotensin II (ref. 3). The two hormone systems are interconnected by the angiotensin-converting enzyme, which releases angiotensin II from its precursor and inactivates the vasodepressor bradykinin4. Here we show that the AT1 receptor and the bradykinin (B2) receptor also communicate directly with each other. They form stable heterodimers, causing increased activation of Gαq and Gαi proteins, the two major signalling proteins triggered by AT1. Furthermore, the endocytotic pathway of both receptors changed with heterodimerization. This is the first example of signal enhancement triggered by heterodimerization of two different vasoactive hormone receptors.

Date: 2000
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DOI: 10.1038/35024095

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