Authors: Carsten A Wagner Olivier Devuyst Soline Bourgeois Nilufar Mohebbi
Publish Date: 2009/03/07
Volume: 458, Issue: 1, Pages: 137-156
Abstract
The renal collecting system serves the finetuning of renal acid–base secretion Acidsecretory typeA intercalated cells secrete protons via a luminally expressed Vtype H+ATPase and generate new bicarbonate released by basolateral chloride/bicarbonate exchangers including the AE1 anion exchanger Efficient proton secretion depends both on the presence of titratable acids mainly phosphate and the concomitant secretion of ammonia being titrated to ammonium Collecting duct ammonium excretion requires the Rhesus protein RhCG as indicated by recent KO studies Urinary acid secretion by typeA intercalated cells is strongly regulated by various factors among them acid–base status angiotensin II and aldosterone and the Calciumsensing receptor Moreover urinary acidification by H+ATPases is modulated indirectly by the activity of the epithelial sodium channel ENaC Bicarbonate secretion is achieved by nontypeA intercalated cells characterized by the luminal expression of the chloride/bicarbonate exchanger pendrin Pendrin activity is driven by H+ATPases and may serve both bicarbonate excretion and chloride reabsorption The activity and expression of pendrin is regulated by different factors including acid–base status chloride delivery and angiotensin II and may play a role in NaCl retention and blood pressure regulation Finally the relative abundance of typeA and nontypeA intercalated cells may be tightly regulated Dysregulation of intercalated cell function or abundance causes various syndromes of distal renal tubular acidosis underlining the importance of these processes for acid–base homeostasisWork in the laboratory of the authors has been supported by grants from the Swiss National Science Foundation and FP6 and FP7 work program projects of the European Community EuReGene EUNEFRON N Mohebbi is the recipient of an ERAEDTA longterm fellowship
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