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- W2012012130 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." @default.
- W2012012130 created "2016-06-24" @default.
- W2012012130 creator A5019935894 @default.
- W2012012130 date "2006-12-01" @default.
- W2012012130 modified "2023-10-13" @default.
- W2012012130 title "Regulation of kidney acid excretion by endothelins" @default.
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- W2012012130 doi "https://doi.org/10.1038/sj.ki.5001905" @default.
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