These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Urotensin II activates sarcolemmal Na+/H+ exchanger in adult rat ventricular myocytes. Author: Kato K, Yasutake M, Jia D, Snabaitis AK, Avkiran M, Kusama Y, Takano T, Mizuno K. Journal: J Cardiovasc Pharmacol; 2010 Feb; 55(2):191-7. PubMed ID: 20040885. Abstract: OBJECTIVES: Our aims in the present study were (1) to determine the effects of urotensin II (UT-II) on the sarcolemmal Na/H exchanger (NHE1) activity, and (2) to investigate possible kinase pathways for UT-II-mediated NHE1 stimulation. METHODS: In single rat ventricular myocytes (n = 5-10/group) loaded with the pH-sensitive fluoroprobe carboxy-seminaphthorhodafluor-1, acid efflux rates (JH) were determined as an index of NHE1 activity by rate of recovery of intracellular pH (pHi) from NH4Cl-induced acidosis and the intrinsic buffering power. Phosphorylation of extracellular signal-regulated kinase (ERK), a key kinase of NHE1 activation, was determined by Western blot analysis. RESULTS: JH increased by 31%-71% relative to control in the presence of 100 nmol/L UT-II at pHi range of 6.6-7.0. Stimulation of NHE1 activity by UT-II was abolished by inhibitors of phospholipase C, protein kinase C, and ERK kinase; 2-nitro-4-carboxyphenil-N,N-diphenilcarbamate at 100 micromol/L, GF109203X at 300 nmol/L, and PD98059 at 50 micromol/L, respectively. Moreover, UT-II at 100 nmol/L produced a significant increase in cellular ERK1/2 phosphorylation, which was also inhibited by those inhibitors. CONCLUSIONS: Our study was the first to demonstrate that UT-II activates the cardiac sarcolemmal NHE1 and that the phenomenon may involve, at least in part, the phospholipase C-protein kinase C-ERK pathway.[Abstract] [Full Text] [Related] [New Search]