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Kidney Int. 2006 Dec;70(12):2066-73. Epub 2006 Oct 4.

Regulation of kidney acid excretion by endothelins.

Author information

1
Division of Nephrology and Hypertension, Departments of Internal Medicine and Physiology, Texas Tech University Health Sciences Center, Lubbock, Texas 79430, USA. donald.wesson@ttuhsc.edu

Abstract

Endothelin (ET) is a potent vasoconstrictor that is now known to modulate kidney tubule transport, including kidney tubule acidification. Animals undergoing an acid challenge to systemic acid-base status and with some models of chronic metabolic acidosis have increased kidney ET production. Increased ET production/activity contributes to enhanced kidney tubule acidification that facilitates kidney acid excretion in response to an acid challenge to systemic acid-base status. The data to date support a physiologic role for ET in mediating enhanced kidney acidification in response to acid challenges, but do not support an ET role in maintaining kidney tubule acidification in control, non-acid-challenged states. ET increases acidification in both the proximal and distal nephron and appears to exert its effects both directly and indirectly, the latter through modulating the levels and/or activity or other mediators of kidney tubule acidification. ET also contributes to enhanced kidney acidification in some pathophysiologic states and might contribute to some untoward outcomes associated with these conditions. Whether ET should be a therapeutic target in treating and/or preventing some of these untoward outcomes remains an open question. This review supports continued research into the physiologic and possibly pathophysiologic role of ET in settings of increased kidney tubule acidification.

PMID:
17021604
DOI:
10.1038/sj.ki.5001905
[Indexed for MEDLINE]
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