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Am J Physiol Heart Circ Physiol 283: H2458-H2465, 2002. First published August 29, 2002; doi:10.1152/ajpheart.00295.2002
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Vol. 283, Issue 6, H2458-H2465, December 2002

Endothelin-1 increases calcium and attenuates renin gene expression in As4.1 cells

Michael J. Ryan1, Thomas A. Black2, Susan L. Millard3, Kenneth W. Gross2, and George Hajduczok1

1 Department of Physiology and Biophysics and 3 Pharmacology and Toxicology, State University of New York at Buffalo, Buffalo 14214; and 2 Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York 14263

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 by using a renin-producing cell line As4.1. ET-1 caused an increase in As4.1 cell intracelluar Ca2+ concentration ([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 with an EC50 of 2.1 nM. ET-1 reduced renin mRNA by 68% independently of changes in message decay. With the use of a renin-luciferase reporter system in As4.1 cells, ET-1 reduced luciferase activity by 51%, suggesting that renin gene transcription is directly modified by ET-1.

renin; endothelin; transcription; nitric oxide


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