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- W2043953269 abstract "A series of pharmaceutical successes in the treatment of not only essential hypertension but also vascular hypertrophic and hyperplastic diseases, congestive heart failure, and renal degenerative diseases, with angiotensin-converting enzyme inhibitors and angiotensin (Ang) II receptor antagonists indicates that angiotensin may play a pivotal role in the genesis and maintenance of high blood pressure and resultant stroke, atherosclerosis, and heart and kidney diseases. There is more than one form of Ang II receptors. Using expression cloning, we isolated the AT1 cDNA from bovine adrenocortical cells from the kidney of spontaneously hypertensive rats and AT2 cDNA from rat PC12W cells and we showed that it was not the mas oncogene product. Further, we showed that in rodents, AT1 consists of two subtypes, AT1a and AT1b, which share a high degree of sequence homology in their coding regions, although mechanisms of their respective transcriptional control seemed to be different. By computer-assisted modeling and site-directed mutagenesis, we have delineated the docking site of Ang II. AT1a (and AT1b) serves most of the commonly recognized actions of Ang II. In addition, this G protein-coupled receptor (GPCR) also activates a tyrosine kinase mechanism that may be an underlying cause of Ang II-mediated hypertrophic and hyperplastic changes of cardiovascular tissues. In the vascular system, the phospholipase C (PLC) activated by Ang II seems to be PLC-β rather than PLC-γ1." @default.
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- W2043953269 date "1998-01-01" @default.
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- W2043953269 title "Angiotensin II Receptors AT1 and AT2: New Mechanisms of Signaling And Antagonistic Effects of AT1 and AT2" @default.
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- W2043953269 doi "https://doi.org/10.1007/978-1-4615-5743-2_11" @default.
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