POTASSIUM-DEPLETION AND ACID-BASE TRANSPORTERS IN RAT-KIDNEY - DIFFERENTIAL EFFECT OF HYPOPHYSECTOMY

Citation
Zh. Wang et al., POTASSIUM-DEPLETION AND ACID-BASE TRANSPORTERS IN RAT-KIDNEY - DIFFERENTIAL EFFECT OF HYPOPHYSECTOMY, American journal of physiology. Renal, fluid and electrolyte physiology, 41(6), 1997, pp. 736-743
Citations number
46
Categorie Soggetti
Physiology
ISSN journal
03636127
Volume
41
Issue
6
Year of publication
1997
Pages
736 - 743
Database
ISI
SICI code
0363-6127(1997)41:6<736:PAATIR>2.0.ZU;2-T
Abstract
Potassium depletion is involved in the pathophysiology of metabolic al kalosis. In the present study, the expression of renal acid-base trans porters that are involved in HCO, reabsorption was studied in potassiu m depletion. Rats fed potassium-deficient (KD) diet developed signific ant hypokalemia at 14 days (serum K+ 1.9 +/- 0.2 in KD vs. 4.2 +/- 0.2 meq/l in control, P < 0.01) but not at 6 days (3.8 +/- 0.3 in KD vs. 4.1 +/- 0.3 meq/l in control, P > 0.05). Kidney mRNA for colonic H+-K-adenosinetriphosphatase (H+-K+-ATPase, cHKA) increased by similar to 3- and 11-fold at 6 and 14 days of KD diet, respectively, indicating t hat increased expression preceded the onset of hypokalemia. The expres sion of Na+/H+ exchanger 3 (NHE-3) mRNA and its cognate protein remain ed unchanged at 6 and 14 days of KD diet. The mRNA levels for NHE-1, N HE-2, and NHE-4 also remained unchanged at 6 and 14 days of KD diet. H ypophysectomized (HPX) rats fed KD diet for 14 days developed similar hypokalemia. However, the expression of cHKA mRNA in the kidney was de creased by similar to 80% in potassium-depleted (HPX + KD) rats (P < 0 .01 vs. KD only). Hypophysectomy did not affect the mRNA levels for ei ther gastric H+-K+-ATPase (gHKA) or NHE isoforms in KD animals. Thus p otassium depletion increases expression of cHKA in the kidney but not that of gHKA or NHE isoforms. The signal for this increase appears to precede hypokalemia. Furthermore, the data suggest that pituitary horm one(s) plays an important and novel role in the regulation of cHKA.