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Am J Physiol Regul Integr Comp Physiol 284: R674-R681, 2003. First published November 7, 2002; doi:10.1152/ajpregu.00589.2002
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Vol. 284, Issue 3, R674-R681, March 2003

Unique endothelin receptor binding in kidneys of ETB receptor deficient rats

Traci A. Taylor1, Cheryl E. Gariepy2, David M. Pollock3,4, and Jennifer S. Pollock1,3

Departments of 1 Pharmacology and Toxicology and 4 Surgery, 3 Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912; and 2 Department of Pediatrics, University of Michigan, Ann Arbor, Michigan 48109

Gariepy and colleagues (Gariepy CE, Williams SC, Richardson JA, Hammer RE, and Yanagisawa M. J Clin Invest 102: 1092-1101, 1998.) developed rescued spotting-lethal rats that carry a naturally occurring deletion of the endothelin (ET) type B receptor gene resulting in a lack of functional renal ETB receptor expression. It has been shown that rats homozygous (sl/sl) for the deletion have elevated plasma ET-1 levels; thus, the purpose of this study was to determine whether this deletion would result in a downregulation of ETA receptors in renal tissue. ET-1 and ET-3 binding experiments were performed with cortex, outer medullary, and inner medullary membranes of heterozygous (sl/+) and sl/sl ETB receptor-deficient rats. 125I-labeled ET-1 binding in sl/sl cortex and outer medulla was significantly lower than cortex and outer medulla from sl/+ rats. In contrast to sl/+ rats, [125I]ET-3 binding was not detected in the cortex and outer medulla of sl/sl rats, indicating a lack of ETB receptor expression. The inner medulla of sl/+ rats also demonstrated an abundance of ETB receptors. Surprisingly, however, we also observed significant [125I]ET-3 binding in the sl/sl inner medulla. Furthermore, ET-3 binding in the inner medulla could be blocked with an ETA receptor antagonist in sl/sl rats but not in tissue from sl/+ rats. These studies indicate that rats deficient in ETB receptors have decreased renal cortical and outer medullary ETA receptor number, most likely in response to elevated plasma ET-1 levels. In addition, homozygous ETB-deficient rats express a novel inner medullary ET-3 binding site.

endothelin B receptor; kidney; receptor binding; spotting-lethal rats


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