Document Detail

The regulation of renal acid secretion: new observations from studies of distal nephron segments.
MedLine Citation:
PMID:  3528609     Owner:  NLM     Status:  MEDLINE    
In this review we have attempted to present for the general reader the new information on renal acidification that has emerged from the study of discrete segments of the distal nephron. We have structured our presentation in the context of the cation exchange hypothesis which has strongly influenced modern thinking of acid-base regulation. We have shown that distal nephron acidification is active and can proceed even in the absence of sodium. We have also shown beyond doubt, that pH or the determinants of pH can influence the rate of proton secretion in probably all of the distal nephron segments. We have drawn attention to an exciting new means by which chloride (or its substitution) could alter the rate of net bicarbonate transport. A possible role for bicarbonate secretory activity in the mammalian distal nephron has been discussed as has the influence of mineralocorticoids on acid secretion. There is no question that all of this new information has created the need for a reassessment of the validity of the cation exchange hypothesis. After all, this is a view which specifically denies that renal acid excretion is modulated by pH of the blood, and affirms that it is intrarenal sodium handling that is the "driving force", so to speak, behind acidification responses. However, it seems inappropriate at this time to insist that current data do not allow for a component of sodium transport by the distal nephron to modulate the rate of acid secretion. It is also possible, as we have suggested, that an important effect of chloride gradients, independent of blood pH, could alter bicarbonate retrieval. Most importantly, we wish to stress that much of the in vitro perfusion data does not derive from animals subjected to the chronic acid-base derangements which were precisely those situations to which the cation exchange hypothesis was directed. Simply put, the whole animal studies of Schwartz and his colleagues provided no experimental observations on intrarenal sodium handling or acidification mechanisms, just as the microperfusion studies, both in vivo and in vitro, provide insufficient data that can be applied to whole animals subjected to chronic disturbances.(ABSTRACT TRUNCATED AT 400 WORDS)
D Z Levine; H R Jacobson
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Kidney international     Volume:  29     ISSN:  0085-2538     ISO Abbreviation:  Kidney Int.     Publication Date:  1986 Jun 
Date Detail:
Created Date:  1986-09-26     Completed Date:  1986-09-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1099-109     Citation Subset:  IM    
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MeSH Terms
Acid-Base Equilibrium*
Aldosterone / physiology
Anions / physiology
Anura / physiology
Bicarbonates / metabolism
Biological Transport, Active
Chlorides / physiology
Hydrogen-Ion Concentration
Kidney / physiology*
Kidney Tubules, Collecting / physiology
Membrane Potentials
Sodium / physiology*
Turtles / physiology
Urinary Bladder / physiology
Reg. No./Substance:
0/Anions; 0/Bicarbonates; 0/Chlorides; 52-39-1/Aldosterone; 7440-23-5/Sodium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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