Nox1 upregulates the function of vascular T-type calcium channels following chronic nitric oxide deficit
Cardiovascular disease is characterised by reduced nitric oxide bioavailability resulting from oxidative stress. Our previous studies have shown that nitric oxide deficit per se increases the contribution of T-type calcium channels to vascular tone through increased superoxide from NADPH oxidase (Nox). The aim of the present study was therefore to identify the Nox isoform responsible for modulating T-type channel function, as T-type channels are implicated in several pathophysiological...[Show more]
|Collections||ANU Research Publications|
|Source:||Pflugers Archives European Journal of Physiology|
|01_Howitt_Nox1_upregulates_the_function_2014.pdf||641.1 kB||Adobe PDF||Request a copy|
Items in Open Research are protected by copyright, with all rights reserved, unless otherwise indicated.