Home HOME General Physiology and Biophysics 2009 General Physiology and Biophysics Vol.28, No.3, p.225-232, 2009

Journal info


Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

Aims and Scope
Editorial Info
Abstracting and Indexing
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.28, No.3, p.225-232, 2009

Title: Effect of 7-nitroindazole on the expression of intracellular calcium channels in the kidney of spontaneously hypertensive rats
Author: Barbora Sedlakova, Sona Cacanyiova, Karol Ondrias, Frantisek Kristek and Olga Krizanova

Abstract:  The spontaneously hypertensive rats (SHR) were fed with nitric oxide synthase (NOS) blocker 7-nitroindazole (7-NI, 10 mg/kg/day) for 6 weeks and an expression of intracellular calcium channels, SERCA and proapoptotic agents was evaluated in kidney. Treatment of rats with 7-NI resulted in a significant increase in mRNA and protein levels of the IP3 receptors type 1 and type 2, while mRNA levels of the IP3 receptor type 3 remained unchanged. The mRNA of other intracellular calcium channels, ryanodine receptors type 1 and type 2 was also upregulated by 7-NI treatment. Gene expression of the SERCA2a, calcium pump responsible for loading intracellular stores with calcium, revealed increased gene expression due to 7-NI as well. Interestingly, proapoptotic agents caspase 3 and Bax were also upregulated by the 7-NI treatment. These results may indicate that nNOS blocker 7-NI modifies intracellular calcium transport system, which may have impact on altered calcium handling and regulation of various metabolic pathways.

Keywords: IP3 receptors — 7-nitroindazole — Spontaneously hypertensive rats — Apoptosis
Year: 2009, Volume: 28, Issue: 3 Page From: 225, Page To: 232
doi:10.4149/gpb_2009_03_225


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.