Abstract
Nerol (C10H18O) is a monoterpene found in many essential oils, such as lemon balm and hop. In this study, we explored the contractile and electrophysiological properties of nerol and demonstrated its antiarrhythmic effects in guinea pig heart preparation. Nerol effects were evaluated on atrial and ventricular tissue contractility, electrocardiogram (ECG), voltage-dependent L-type Ca2+ current (ICa,L), and ouabain-triggered arrhythmias. Overall our results revealed that by increasing concentrations of nerol (from 0.001 to 30 mM) there was a significant decrease in left atrium contractile force. This effect was completely and rapidly reversible after washing out (~ 2 min). Nerol (at 3 mM concentration) decreased the left atrium positive inotropic response evoked by adding up CaCl2 in the extracellular medium. Interestingly, when using a lower concentration of nerol (30 μM), it was not possible to clearly observe any significant ECG signal alterations but a small reduction of ventricular contractility was observed. In addition, 300 μM nerol promoted a significant decrease on the cardiac rate and contractility. Important to note is the fact that in isolated cardiomyocytes, peak ICa,L was reduced by 58.9 ± 6.31% after perfusing 300 μM nerol (n=7, p<0.05). Nerol, at 30 and 300 μM, delayed the time of onset of ouabain-triggered arrhythmias and provoked a decrease in the diastolic tension induced by the presence of ouabain (50 μM). Furthermore, nerol preincubation significantly attenuated arrhythmia severity index without changes in the positive inotropism elicited by ouabain exposure. Taken all together, we may be able to conclude that nerol primarily by reducing Ca2+ influx through L-type Ca2+ channel blockade lessened the severity of ouabain-triggered arrhythmias in mammalian heart.
Highlights
Cardiac arrhythmia is caused by changes in the coordinated electrical activity of the heart and is surely among the leading causes of sudden death in the modern world [1, 2]
Ouabain-triggered arrhythmias is based on disturbances in the intracellular Ca2+ handling, overload of Ca2+, and unbalance of Na+/Ca2+ exchanger activity (NCX) [5]
We investigated the occurrence of subtypes of ventricular arrhythmias, such as ventricular premature beats (VPB), ventricular tachycardia (VT), and/or ventricular fibrillation (VF)
Summary
Cardiac arrhythmia is caused by changes in the coordinated electrical activity of the heart and is surely among the leading causes of sudden death in the modern world [1, 2]. Cardiac myocytes exhibit an exquisite dynamic control of intracellular Ca2+ homeostasis. Perturbations in this control process have been recognized as a major contributor to lifethreatening ventricular arrhythmias [4]. In this very aspect the model of arrhythmias induced by exposure of heart tissue to ouabain (which is per se a natural product) is an excellent and straightforward approach for the study of the putative antiarrhythmic activity of natural products. Ouabain-triggered arrhythmias is based on disturbances in the intracellular Ca2+ handling, overload of Ca2+, and unbalance of Na+/Ca2+ exchanger activity (NCX) [5]. Recent studies have reported that cardiac hypertrophy and heart failure may be associated with increased arrhythmogenic risk by the enhanced NCX activity [6, 7]
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