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[1]M. H. Weinberger, J. Z. Miller, F. C. Luft, C. E. Grim and N. S. Fineberg: Definitions and characteristics of sodium sensitivity and blood pressure resistance. Hypertension, 8(6 Pt 2), II127-34 (1986)
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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.
Regulation and function of renal medullary cyclooxygenase-2 during high salt loading
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
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
References
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