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Dr. Sian E. Harding
The strongest impression generated during this engrossing session, which I co-chaired with Dr Arshed A. Quyyumi (Atlanta, USA), was the multiplicity of nitric oxide (NO)-dependent mechanisms open to therapeutic targeting for heart disease.
Presenters described control by the constitutive NO synthase isoforms eNOS and nNOS in platelets and vessel walls (Prof Lina Badimon, Barcelona, Spain), endothelial progenitor cells and bone marrow stromal cells (Prof Pieter Doevendans, Utrecht, and The Netherlands), sympathetic and parasympathetic nerves (Prof David Patterson, Oxford, UK) in addition to the oxygen consumption of the cardiac myocyte (Prof Akos Koller, Budapest, Hungary). The implications for applications of NO modulation in thrombosis, hypertension, myocardial failure and hyperhomocysteinaemia were elaborated by each speaker. Prof Badimon described studies which drew the perfect arc from hypothesis-based cell and animal research through to the use of prospective therapeutic agents in man, with the demonstration of an antithrombotic effect of new NO donors. Benefit was shown even in addition to aspirin plus clopidogrel, underlining the distinct mechanism of action of the new compounds. Importantly, a clear separation could be obtained between the antithrombotic and hypotensive effects, allowing the potential for compounds which will be selective to prevent accretion of platelets without a dangerous drop in blood pressure. On the other end of the translational axis, Prof Doevedans described the central role of NO in homing and retention of endothelial progenitor cells in cardiac repair. As for all the speakers, the talk moved between highly detailed basic science and human studies for an exemplary demonstration of the full translational spectrum.
Because of the pleiotropic nature of NO, harnessing the full therapeutic power of NO modulation will depend on finding ways to target tissues and even subcellular locations more specifically than the current NO donors and isoform specific NO synthase inhibitors can do. The description of an antithrombotic NO donor with reduced hypotensive effects shows that this is indeed possible.
Therapeutic potential of nitric oxide (NO): NO news, good news Symposium - Bench to Bedside
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