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Articles in PresS, published online ahead of print August 29, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00295.2002
Submitted on April 3, 2002
Accepted on August 26, 2002
1 Department of Physiology & Biophysics, State University of New York at Buffalo, Buffalo, NY, USA
2 Molecular & Cellular Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
3 Pharmacology & Toxicology, State University of New York at Buffalo, Buffalo, NY, USA
* To whom correspondence should be addressed. E-mail: ryanm{at}physiology.uiowa.edu.
Endothelin-1 (ET-1) is a potent vasoconstrictor and blood pressure modulator. Renin secretion from juxtaglomerular (JG) cells is crucial for blood pressure and electrolyte homeostasis and has been shown to be modulated by ET-1 however the cellular and molecular mechanism of this regulation is not clear. The purpose of this study was to gain a better understanding of the cellular and molecular pathways activated by ET-1 using a renin producing cell line, As4.1. ET-1 caused an increase in As4.1 cell [Ca2+]i mediated by the ETA receptor, as its antagonist, BQ-123 abolished the response. The nitric oxide donor, nitroprusside but not 8-Bromo cGMP, reduced the time necessary for successive ET-1 responses. Endothelin-3 had no effect on [Ca2+]i. ET-1 dose dependently increased total inositol phosphates (IP) with an EC50 of 2.1 nM. ET-1 reduced renin mRNA by 68% independently of changes in message decay. Using a renin-luciferase reporter system in As4.1 cells, ET-1 reduced luciferase activity by 51% suggesting that rennin gene transcription is directly modified by ET-1.
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