Altered expression of renal bumetanide-sensitive sodium-potassium-2 chloride cotransporter and Cl- channel -K2 gene in angiotensin II-infused hypertensive rats.
- Author:
Tao YE
1
;
Zhi-quan LIU
;
Chao-feng SUN
;
Yong ZHENG
;
Ai-qun MA
;
Yuan FANG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Animals; Blood Pressure; drug effects; Gene Expression Regulation; drug effects; Hypertension; chemically induced; metabolism; Male; RNA, Messenger; analysis; Rats; Rats, Sprague-Dawley; Sodium-Potassium-Chloride Symporters; genetics; Solute Carrier Family 12, Member 1
- From: Chinese Medical Journal 2005;118(23):1945-1951
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDLittle information is available regarding the effect of angiotensin II (Ang II) on the bumetanide-sensitive sodium-potassium-2 chloride cotransporter (NKCC2), the thiazide-sensitive sodium-chloride cotransporter (NCC), and the Cl- channel (CLC)-K2 at both mRNA and protein expression level in Ang II-induced hypertensive rats. This study was conducted to investigate the influence of Ang II with chronic subpressor infusion on nephron-specific gene expression of NKCC2, NCC and CLC-K2.
METHODSSprague Dawleys rats were treated subcutaneously with either Ang II (100 ng.kg-1.min-1) or vehicle for 14 days. Expression of NKCC2, NCC and CLC-K2 mRNA in kidneys was determined by real time polymerase chain reaction (PCR). Western blotting analysis was used to measure NKCC2 and NCC protein expression.
RESULTSAng II significantly increased blood pressure and up-regulated NKCC2 mRNA and protein expression in the kidney. Expression of CLC-K2 mRNA in the kidney increased 1.6 fold (P < 0.05). There were no changes in NCC mRNA or protein expression in AngII-treated rats versus control.
CONCLUSIONSChronic subpressor Ang II infusion can significantly alter NKCC2 and CLC-K2 mRNA expression in the kidney, and protein abundance of NKCC2 in kidney is positively regulated by Ang II. These effects may contribute to enhanced renal Na+ and Cl- reabsorption in response to Ang II.
