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Am J Physiol Renal Physiol (April 12, 2005). doi:10.1152/ajprenal.00003.2005
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Submitted on January 6, 2005
Accepted on April 4, 2005

Enhanced Expression of EGF Receptor in a Model of Salt-Sensitive Hypertension

Wei-Zhong Ying1 and Paul W. Sanders2*

1 Department of Medicine and Department of Veterans Affairs Medical Center, University of Alabama at Birmingham, Birmingham, AL, USA
2 Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, AL, USA

* To whom correspondence should be addressed. E-mail: psanders{at}uab.edu.

Chronic kidney disease in the Dahl/Rapp salt-sensitive (S) rat is related to an arteriolopathic process that occurs following the onset of hypertension and involves vascular smooth muscle cell (VSMC) hyperplasia and luminal constriction. Because previous studies have shown that activation of the epidermal growth factor receptor (EGFR) produces a mitogenic stimulus in VSMC and the EGFR participates integrally in the vasoconstrictor responses of renal arterioles, the present study analyzed the expression of EGFR in these animals. Compared to Sprague-Dawley (SD) rats, renal cortical expression of EGFR was increased in both prehypertensive and hypertensive S rats. Immunohistochemistry using a polyclonal antibody to EGFR demonstrated that EGFR expression was prominent in the renal vasculature, particularly in the media of afferent and efferent arterioles and the aorta of S rats. When examined, primary cultures of VSMC from S rats showed increased expression of EGFR, compared to VSMC from SD and Dahl/Rapp salt-resistant (R) rats. Following addition of EGF, autophosphorylation of the EGFR was enhanced in cells from S rats, as was the downstream signaling events that included activation of p42/44 mitogen-activated protein kinase (MAPK) and Akt pathways. Thus, in vivo and in vitro studies demonstrated augmented expression and functional activity of the EGFR in S rats.




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