In this study, the vasodilatory actions of nine edible tropical plant extracts were investigated. Ipomoea batatas (sweet potato leaf), Piper betle (betel leaf), Anacardium occidentale (cashew leaf), Gynandropsis gynandra (maman leaf), Carica papaya (papaya leaf), and Mentha arvensis (mint leaf) extracts exhibited more than 50% relaxing effect on aortic ring preparations, while Piper betle and Cymbopogon citratus (lemongrass stalk) showed comparable vasorelaxation on isolated perfused mesenteric artery preparation. The vascular effect on the aortic ring preparations were mainly endothelium-dependent, and mediated by nitric oxide (NO) as supported by the inhibition of action in the presence of N(omega)-nitro-L-arginine (NOLA), an nitric oxide synthase (NOS) inhibitor, or by the removal of endothelium. In contrast, vasodilatory actions in resistance vessels (perfused mesenteric vascular beds) appear to involve several biochemical mediators, including NO, prostanoids, and endothelium-dependent hyperpolarizing factors (EDHFs). Total phenolic contents and antioxidant capacities varied among different extracts and found to be independent of vascular relaxation effects. This study demonstrates that many edible plants common in Asian diets to possess potential health benefits, affording protection at the vascular endothelium level.

The concept that diet-induced changes in membrane lipids could modify heart function partly arose from observations that membrane composition and physical properties were closely associated with the capacity of the heart to respond appropriately to torpor and hibernation. Observations of natural hibernators further revealed that behavior of key membrane-bound enzymes could be influenced through the lipid composition of the cell membrane, either by changing the surrounding fatty acids through reconstitution into a foreign lipid milieu of different composition, or by alteration through diet. Myocardial responsiveness to beta-adrenoceptor stimulation, including initiation of spontaneous dysrhythmic contractions, was altered by both hibernation and dietary modulation of membrane fatty acids, suggesting modified vulnerability to cardiac arrhythmia. Subsequent studies using whole-animal models recognized that vulnerability to ventricular fibrillation decreased as the polyunsaturated: saturated fat (P:S) ratio of the diet increased. However, dietary fish oils, which typically contain at least 30% saturated fatty acids and only 30% long-chain n-3 (omega-3) polyunsaturated fatty acids (PUFA), exhibit antiarrhythmic effects that exceed the predicted influence of the P:S ratio, suggesting properties unique to the long-chain n-3 PUFA. Large-scale clinical trials and epidemiology have confirmed the arrhythmia prevention observed in vitro in myocytes, papillary muscles, and isolated hearts and in whole-animal models of sudden cardiac death. Some progress has been made towards a biologically plausible mechanism. These developments highlight nature's ability to provide guidance for the most unexpected applications.

Regular fish or fish oil intake is associated with a low incidence of heart failure clinically, and fish oil-induced reduction in cardiac remodelling seen in hypertrophy models may contribute. We investigated whether improved cardiac energy efficiency in non-hypertrophied hearts translates into attenuation of cardiac dysfunction in hypertrophied hearts. Male Wistar rats (n 33) at 8 weeks of age were shamoperated or subjected to abdominal aortic stenosis to produce pressure-overload cardiac hypertrophy. Starting 3 weeks post-operatively to follow initiation of hypertrophy, rats were fed a diet containing 10 % olive oil (control) or 5 % fish oil (ROPUFAw 30 (17 % EPA, 10 % DHA)) þ 5 % olive oil (FO diet). At 15 weeks post-operatively, ventricular haemodynamics and oxygen consumption were evaluated in the blood-perfused, isolated working heart. Resting and maximally stimulated cardiac output and external work were .60 % depressed in hypertrophied control hearts but this was prevented by FO feeding, without attenuating hypertrophy. Cardiac energy efficiency was lower in hypertrophy, but greater in FO hearts for any given cardiac mass. Coronary blood flow, restricted in hypertrophied control hearts, increased with increasing work in hypertrophied FO hearts, revealing a significant coronary vasodilator reserve. Pronounced cardiac dysfunction in hypertrophied hearts across low and high workloads, indicative of heart failure, was attenuated by FO feeding in association with membrane incorporation of n-3 PUFA, principally DHA. Dietary fish oil may offer a new approach to balancing the high oxygen demand and haemodynamic requirements of the failing hypertrophied heart independently of attenuating hypertrophy.