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Articles in PresS, published online ahead of print November 7, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00589.2002
Submitted on September 20, 2002
Accepted on October 31, 2002
1 Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia, USA
2 Department of Pediatrics, University of Michigan, Ann Arbor, Michigan, USA
3 Vascular Biology Center, Medical College of Georgia, Augusta, Georgia, USA; Department of Surgery, Medical College of Georgia, Augusta, Georgia, USA
4 Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia, USA; Vascular Biology Center, Medical College of Georgia, Augusta, Georgia, USA
* To whom correspondence should be addressed. E-mail: jpollock{at}mail.mcg.edu.
Gariepy and colleagues developed rescued spotting-lethal rats that carry a naturally occurring deletion of the ETB receptor gene resulting in a lack of 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 down-regulation 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]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.
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