IMR Press / FBL / Volume 22 / Issue 1 / DOI: 10.2741/4476

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review

Regulation and function of renal medullary cyclooxygenase-2 during high salt loading

Show Less
1 Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah and Institute of Hypertension, Sun Yat-sen University School of Medicine, Guangzhou, 510080, China
Academic Editor:Pin-Lan Li
Front. Biosci. (Landmark Ed) 2017, 22(1), 128–136; https://doi.org/10.2741/4476
Published: 1 January 2017
(This article belongs to the Special Issue Molecular pathobiology of lipid mediators)
Abstract

Prostaglandins (PGs) are important autocrine/paracrine regulators that contribute to sodium balance and blood pressure control. Along the nephron, the highest amount of PGE2 is found in the distal nephron, an important site for fine-tuning of urinary sodium and water excretion. Cylooxygenase-2 (COX-2) is abundantly expressed in the renal medulla and its expression along with urinary PGE2 excretion is highly induced by chronic salt loading. Factors involved in high salt-induced COX-2 expression in the renal medulla include the hypertonicity, fluid shear stress (FSS), and hypoxia-inducible factor-1α (HIF-1α). Site-specific inhibition of COX-2 in the renal medulla of Sprague-Dawley rats causes sodium retention and salt-sensitive hypertension. Together, these results support the concept that renal medullary COX-2 functions an important natriuretic mediator that is activated by salt loading and its products promote sodium excretion and contribute to maintenance of sodium balance and blood pressure.

Keywords
COX-2
Prostaglandin E2
Hypertonicity
Hypoxia-Inducible Factor-1 Alpha
Fluid Shear Stress
Blood Pressure
Review
Share
Back to top