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Review details post-translational regulation and rapid desensitization of Ang II receptors following agonist stimulation.
This review summarizes mechanisms of post-translational regulation and rapid desensitization of the AT1 angiotensin receptor following agonist stimulation.
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AT1 desensitization mechanisms clarified in cell models; leaves open relevance to clinical RAAS inhibitor responses.
Angiotensin II is an eight amino acid peptide which plays a major role in the regulation of cardiovascular homeostasis. The physiologic effects of angiotensin (Ang) II are mediated by a G-protein coupled receptor, termed AT1, which activates phospholipase C. A major factor regulating angiotensin II receptor function is the rapid desensitization following agonist stimulation. However, despite years of investigation, the mechanism by which the angiotensin receptor is regulated remains unclear. The cloning of the AT-1 receptor and the availability of cell lines which stabily express this receptor has helped elucidate these mechanisms. In this paper, we review the data from our laboratory concerning the post-translational regulation of the angiotensin receptor function.
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Sasamura et al. (1994) conducted a review in Angiotensin receptor function. Angiotensin II receptor regulation was evaluated. This review summarizes data concerning the post-translational regulation and rapid desensitization of the angiotensin II receptor following agonist stimulation.
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