AJP - Renal AJP: Heart and Circulatory Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol 245: F349-F358, 1983;
0363-6127/83 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kornandakieti, C.
Right arrow Articles by Tannen, R. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kornandakieti, C.
Right arrow Articles by Tannen, R. L.

AJP - Renal Physiology, Vol 245, Issue 3 349-F358, Copyright © 1983 by American Physiological Society


ARTICLES

Hydrogen ion secretion by the rat distal nephron: adaptation to chronic alkali and acid ingestion

C. Kornandakieti, R. Grekin and R. L. Tannen

Isolated rat kidneys perfused at a low bicarbonate concentration were subjected to increased rates of buffer excretion, provided as creatinine, in order to examine the maximal hydrogen ion secretory capacity of the distal nephron. Preliminary experiments with kidneys from normal rats indicated that the quantity of hydrogen ion that titrated creatinine from urine pH to a pH of 6.0, designated TA-pH 6.0, provided an index of net hydrogen ion secretion by a functional segment of the distal nephron. With this technique the response of distal nephron hydrogen ion transport to ingestion of both acid and alkali loads was examined. Perfused kidneys from rats with chronic metabolic acidosis, produced by drinking 1.5% NH4Cl for 3-5 days, excreted urine with a lower pH and higher total titratable acid and TA-pH 6.0 than appropriate controls. Perfused kidneys from rats that ingested NaHCO3 for 7 days exhibited a higher urine pH and lower rates of total titratable acid and TA-pH 6.0 than controls. By contrast, kidneys from rats acutely tube-fed NaHCO3 3 h prior to study showed no change in urinary acidification parameters. Thus, chronic ingestion of an acid load stimulates, and chronic ingestion of an alkali load inhibits, the intrinsic hydrogen ion secretory capacity of the rat kidney at a distal nephron site. This intrinsic adaptation of the hydrogen ion transport mechanism is not secondary to changes in aldosterone because rats that ingested NaHCO3 chronically had higher plasma aldosterone levels than controls.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online