Skip Navigation

Cardiovascular Research 2001 51(1):51-58; doi:10.1016/S0008-6363(01)00241-3
© 2001 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Bryant, S. M
Right arrow Articles by Casadei, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bryant, S. M
Right arrow Articles by Casadei, B.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2000, European Society of Cardiology

Nitric oxide does not modulate the hyperpolarization-activated current, If, in ventricular myocytes from spontaneously hypertensive rats

Simon M Bryanta,*, Claire E Searsa, Lauren Riggb, Derek A Terrarb and Barbara Casadeia

aDepartment of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DU, UK
bDepartment of Pharmacology, Mansfield Road, University of Oxford, Oxford, OX1 3QT, UK

* Corresponding author. Tel.: +44-1865-220-133; fax: +44-1865-221-977 simon.bryant{at}cardiov.ox.ac.uk

Objective: In sinoatrial (SA) node cells, nitric oxide (NO) exerts a dual effect on the hyperpolarization-activated current, If, i.e. in basal conditions NO enhances If whereas in the presence of β-adrenergic stimulation it decreases it. Recent studies have shown that If is present in ventricular myocytes from hypertrophied or failing hearts where it may promote abnormal automaticity. Since these pathological conditions are associated with increased sympathetic tone and upregulation of myocardial NO production, we set out to investigate whether If is similarly modulated by NO in hypertrophied ventricular myocytes. Methods: Left ventricular myocytes were isolated from 18–20-month-old spontaneously hypertensive rats (SHRs). Membrane current was measured under whole-cell or amphotericin-perforated patch-clamp conditions, at 35°C. Results: Application of diethylamine–NO (DEA–NO, 1–100 µM) did not alter the amplitude or voltage dependence of activation of If under basal conditions (half-activation voltage, Vh: control –82.9±2.6, DEA–NO –84.0±2.6 mV). Similarly, If was not affected by the inhibition of endogenous NO production (L-NMMA, 500 µM) or guanylate cyclase (ODQ, 10 µM). Forskolin (10 µM) or isoprenaline (100 nM) elicited a positive shift in Vh but subsequent application of DEA–NO did not further affect the properties of If. Conclusions: Our results show that, unlike in SA node cells, in SHR ventricular myocytes basal and adrenergically stimulated If is not modulated by exogenous NO or by constitutive NO or cGMP production.

KEYWORDS Adrenergic (ant)agonists; Arrhythmia (mechanisms); Hypertrophy; Ion channels; Myocytes; Nitric oxide


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
N. Herring, L. Rigg, D. A Terrar, and D. J Paterson
NO-cGMP pathway increases the hyperpolarisation-activated current, If, and heart rate during adrenergic stimulation
Cardiovasc Res, December 1, 2001; 52(3): 446 - 453.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.