Creat membership Creat membership
Sign in

Forgot password?

Confirm
  • Forgot password?
    Sign Up
  • Confirm
    Sign In
Creat membership Creat membership
Sign in

Forgot password?

Confirm
  • Forgot password?
    Sign Up
  • Confirm
    Sign In
Collection
For ¥0.57 per day, unlimited downloads CREATE MEMBERSHIP Download

toTop

If you have any feedback, Please follow the official account to submit feedback.

Turn on your phone and scan

home > search >

Angiotensin II potentiates the slow component of delayed rectifier K+ current via the AT(1) receptor in guinea pig atrial myocytes

Author:
Zankov, DP  Omatsu-Kanbe, M  Isono, T  Toyoda, F  Ding, WG  Matsuura, H  Horie, M  


Journal:
CIRCULATION


Issue Date:
2006


Abstract(summary):

Background - Angiotensin II (Ang II) has diverse actions on cardiac electrical activity. Little information is available, however, regarding immediate electrophysiological effects of Ang II on cardiac repolarization. Methods and Results - The present study investigated the immediate effects of Ang II on the slow component of delayed rectifier K+ current (I-Ks) and action potentials in guinea pig atrial myocytes using the whole-cell patch-clamp technique. Bath application of Ang II increased the amplitude of I-Ks (EC50, 6.16 nmol/L) concentration dependently. The stable analogue Sar(1)-Ang II was also effective at increasing IKs. The voltage dependence of IKs activation and the kinetics of deactivation were not significantly affected by these agonists. The enhancement of IKs was blocked by the Ang II type 1 (AT(1)) receptor antagonist valsartan (1 mu mol/L) and was markedly attenuated by inclusion of GDP beta S (2 mmol/L) in the pipette, indicating an involvement of G protein - coupled AT1 receptor. The stimulatory effect was also significantly reduced by the phospholipase C inhibitor compound 48/80 (100 mu mol/L) and the protein kinase C inhibitors bisindolylmaleimide I (200 nmol/L) and H-7 (10 mu mol/L), suggesting that AT(1) receptor acts through phospholipase C-protein kinase C signaling cascade to potentiate I-Ks. As expected from its stimulatory action on IKs, Sar(1)-Ang II markedly shortened the action potential duration, which could be reversed by valsartan. Conclusions - The potentiation of I-Ks via AT(1) stimulation in atrial myocytes, accompanied by a shortening of the action potential duration, suggests a potential mechanism by which elevated levels of Ang II may promote atrial fibrillation in heart failure and warrants further investigation.


Page:
1278---1286


VIEW PDF

The preview is over

If you wish to continue, please create your membership or download this.

Create Membership

Similar Literature

Submit Feedback

This function is a member function, members do not limit the number of downloads