Startseite Lebenswissenschaften Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin
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Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin

  • M. David Percival , Sylvie Toulmond , Nathalie Coulombe , Wanda Cromlish , Sylvie Desmarais , Susana Liu , René St-Jacques , Jacques Yves Gauthier und Jean-Francois Fournier
Veröffentlicht/Copyright: 24. September 2010
Biological Chemistry
Aus der Zeitschrift Band 391 Heft 12

Abstract

Renin is the first enzyme in the renin-angiotensin-aldosterone system which is the principal regulator of blood pressure and hydroelectrolyte balance. Previous studies suggest that cathepsin B is the activator of the prorenin zymogen. Here, we show no difference in plasma renin activity, or mean arterial blood pressure between wild-type and cathepsin B knockout mice. To account for potential gene compensation, a potent, selective, reversible cathepsin B inhibitor was developed to determine the role of cathepsin B on prorenin processing in rats. Pharmacological inhibition of cathepsin B in spontaneously hypertensive and double transgenic rats did not result in a reduction in renal mature renin protein levels or plasma renin activity. We conclude that cathepsin B does not play a significant role in this process in rodents.


Corresponding author

Received: 2010-6-21
Accepted: 2010-8-17
Published Online: 2010-09-24
Published in Print: 2010-12-01

©2010 by Walter de Gruyter Berlin New York

Heruntergeladen am 19.12.2025 von https://www.degruyterbrill.com/document/doi/10.1515/bc.2010.140/pdf
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