Abstract
CHIP is a recently cloned, corticosteroid-induced gene which evokes K+ channel activity in oocytes (B. Attali, H. Latter, N. Rachamim, and H. Garty. Proc. Natl. Acad. Sci. USA 92: 60926096, 1995). To further characterize the possible role of this gene in epithelial ion transport, we have studied its epithelial distribution and hormonal induction. Northern hybridizations indicate that the zonal distribution of CHIP niRNA in kidney is: papilla » medulla » cortex. High levels of CHIF were also detected in a primary culture from inner medullary collecting duct (IMCD). Perfusing rats with <20 nM aldosterone through osmotic minipumps evoked a 22.4 ± 1.9-fold increase in colonie CHIF. A significant increase was observed 3 h after administrating the corticosteroid, but maximal response was detected only after a 72-h incubation. This response appears to be mineralocorticoid specific; perfusing or injecting rats with maximal doses of dexamethasone did not evoke a further increase in CHIF mRNA. In contrast, high levels of CHIF are expressed in kidney papilla and IMCD primary culture, irrespective of corticosteroid treatment. Thus, like the apical Na+ channel and the H+-K+-adenosinetriphosphatase, CHIF is mineralocorticoid induced in the colon but constitutively expressed in kidney. Copyright & 1996 the American Physialogical Society.
| Original language | English |
|---|---|
| Pages (from-to) | F322-F329 |
| Journal | American Journal of Physiology |
| Volume | 271 |
| Issue number | 2 PART 2 |
| DOIs | |
| State | Published - 1 Jan 1996 |
Keywords
- Inner medullary collecting duct
- Ion transport
- Kidney papilla
- Mineralocorticoid
ASJC Scopus subject areas
- Physiology (medical)