Abstract
Two AT1 receptor subtypes, AT1A and AT1B, have been cloned and sequenced in the rat.15 Although AT1A and AT1B share a high degree (96%) of amino acid homology,3, 5 they may be functionally different. In studies of AT1A and AT1B receptors transfected into COS-7 cells,4 Sanderberg et al have shown that there are dose-related differences during angiotensin II (Ang II)-induced Ca2+ signalling and differences in binding affinity for Ang II agonists and antagonists between AT1A and AT1B. Although it has been noted that AT1 receptor subtypes in the rat brain can be differentially regulated by hormones or changes in dietary sodium,5, 6 gene regulation of the AT1 receptor subtypes in the kidney has not been fully investigated. Considering the key role of the kidney in the control of fluid homeostasis and blood pressure, it is important to understand the regulation of these two distinct receptor genes in the kidney. Such studies could lead to further insights into the relevance of these receptor genes in hypertensive disease states and possibly could lead to the development of new and more specific therapies. In this study, we used Northern blot and in situ hybridization analysis to test the hypothesis that dietary sodium intake differentially regulates gene expression of the AT1A and AT1B receptor subtypes in the kidney.
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