Autonomic control of the heart: going beyond the classical neurotransmitters. Issue 4 (20th November 2014)

• Record Type: Journal Article
• Authors: Herring, Neil
• Is Part Of: Experimental physiology. Volume 100:Issue 4(2015:Apr.)
• Page Start: 354
• Page End: 358
• Publication Date: 2014-11-20
• Subjects: Physiology, Experimental -- Periodicals; 571.0724
• DOI: 10.1113/expphysiol.2014.080184
• Languages: English
• ISSNs: 0958-0670

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="eph1545-sec-0010" sec-type="section"> <title>New Findings</title> <p> <list id="eph1545-list-0001" list-type="bullet"> <list-item> <p> <bold>What is the topic of this review?</bold> </p> <p>This symposium report discusses the evidence for release of cardiac sympathetic cotransmitters in addition to noradrenaline.</p> </list-item> <list-item> <p> <bold>What advances does it highlight?</bold> </p> <p>It highlights the potential role of neuropeptide Y in reducing vagal neurotransmission and directly influencing ventricular myocyte excitability in the presence of β‐receptor blockade.</p> </list-item> </list> </p> </sec> <sec id="eph1545-sec-0020" sec-type="section"> <p>Acute myocardial infarction and congestive cardiac failure are characterized by high levels of cardiac sympathetic drive. In these conditions, sympathetic neurotransmitters such as neuropeptide Y (NPY) can be released in addition to noradrenaline, and plasma levels correlate with infarct size and mortality. Even in the presence of β‐blockers, NPY is able to bind to its own receptors located on cholinergic ganglia and ventricular myocytes. In this symposium report, I review the evidence that NPY can inhibit acetylcholine release during vagus nerve stimulation and limit the subsequent bradycardia. I also present preliminary, as yet unpublished data, demonstrating that NPY may be pro‐arrhythmic by directly influencing ventricular electrophysiology. Targeting NPY receptors pharmacologically may therefore be a useful therapeutic strategy both to reduce heart rate and to prevent arrhythmias in the setting of myocardial infarction and chronic heart failure. Such medications would be expected to act synergistically with β‐blockers, angiotensin‐converting enzyme inhibitors and implantable cardiac devices, such as defibrillators and vagus nerve stimulators.</p> </sec> </abstract>