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European Journal of Heart Failure 2001 3(5):527-534; doi:10.1016/S1388-9842(01)00163-5
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© 2001 European Society of Cardiology

Nitric oxide: not just a negative inotrope

David Sarkara,b,*, Patrick Vallanceb and Sian E. Hardinga

a Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine Dovehouse St, London SW3 6LY, UK
b Centre for Clinical Pharmacology, University College London London, UK

* Corresponding author. Tel.: +44-20-7352-8121, ext. 3313; fax: +44-20-7823-3392. E-mail address: d.sarkar{at}ucl.ac.uk (D. Sarkar)


  Abstract

Nitric oxide (NO) appears to play a role in modulating cardiac function in both health and disease. Early studies in isolated rodent cardiac myocytes demonstrated a depressant effect of NO supplied by NO donors (exogenous) as well as NO generated within myocytes (endogenous). There is increasing evidence for a functional NO generating system within the human myocardium, which appears upregulated in certain disease states. Induction of the high output nitric oxide synthase isoform (iNOS) has been demonstrated in the failing myocardium, though its functional significance remains unproven. More recently published data have contradicted the notion that NO acts solely as a negative inotrope demonstrating positive inotropy in both isolated rodent and human ventricular myocytes in response to a range of NO donors. Different NO donors have different NO release kinetics and generate a range of NO species (NO·, NO+ and NO–) which may interact at a number of subcellular targets. The observed response of any cardiac preparation to an NO donor represents the net effect of activation of different effector targets and may explain the contradictory reported effects of NO. To realise the therapeutic potential of NO will require specific targeting at a subcellular level.

Key Words: Nitric oxide • Myocardium • Nitric oxide synthase isoform

Received December 20, 2000; Revised February 28, 2001; Accepted April 26, 2001


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