EFFECT OF RESPIRATORY-ACIDOSIS AND RESPIRATORY ALKALOSIS ON RENAL TRANSPORT ENZYMES

Citation
S. Eiamong et al., EFFECT OF RESPIRATORY-ACIDOSIS AND RESPIRATORY ALKALOSIS ON RENAL TRANSPORT ENZYMES, The American journal of physiology, 267(3), 1994, pp. 60000390-60000399
Citations number
45
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
267
Issue
3
Year of publication
1994
Part
2
Pages
60000390 - 60000399
Database
ISI
SICI code
0002-9513(1994)267:3<60000390:EORARA>2.0.ZU;2-B
Abstract
We studied the effect of respiratory acidosis and respiratory alkalosi s on acid-base composition and on microdissected renal adenosinetripho sphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypoc apnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collectin g tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate wa s 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging similar to 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameter s and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significa ntly changed, but H-ATPase and Na-K-ATPase activities were decreased b y 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT a lso decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq /l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities we re 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 1 8.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity conti nued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosterone or potassium. These results demons trate that chronic, but not acute, respiratory acidosis stimulates act ivity of both renal proton ATPases. By contrast, both acute and chroni c respiratory alkalosis decrease the two renal proton pumps. The stimu latory effect of hypercapnia and the inhibitory effect of hypocapnia o n the renal ATPases appear to be potassium and aldosterone independent . Although the precise mechanisms for these results are not known, a d irect effect of PCO2, pH, or changes in bicarbonate delivery may be in volved.