MPS 11-07 CARDIOPROTECTIVE ACTIONS OF RED PALM OIL IN SPONTANEOUSLY HYPERTENSIVE RATS

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Abstract

Objective:

Red palm oil (RPO) has been shown to protect the heart in various cardiovascular disease models. The purpose of this study was to investigate whether intake of antioxidant-rich RPO may affect endothelial dysfunction and oxidative stress known as important mediators in the pathophysiology of hypertension as well as proarrhythmic abnormalities of myocardial connexin43 (Cx43) and PKC epsilon (PKCε) signaling, in a model of essential hypertension.

Design and Method:

3 months old male spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY) were fed standard rat chow plus or minus RPO (200ul/day) for 5 weeks. Left ventricular tissue was used to determine protein expression of Cx43, PKCε and antioxidant enzyme- superoxide dismutase 2 (SOD2). Total NOS activity was measured in the aorta and left ventricular tissue. Langendorff-perfused rat heart was used to examine electrically inducible ventricular fibrillation (VF) and post-ischemic reperfusion-induced malignant arrhythmias.

Results:

RPO supplementation significantly reduced blood pressure in SHR and blood glucose in both SHR and WKY. Protein expression of Cx43, PKCε and SOD2 was significantly increased in a group of SHRrpo. These results were associated with decrease of postischemic reperfusion-related ventricular tachycardia and VF inducibility. NOS activity was increased in the aorta but reduced in the hearts of both WKYrpo and SHRrpo compared to their respective controls.

Conclusions:

Results indicate that SHR benefit from RPO intake, particularly due its endothelial function maintenance by improved NO production in the aorta, by apparent anti-arrhythmic and postischemia-related cardioprotective effects and via reduction of oxidative stress. It appears that RPO supplementation in combination with antihypertensive drugs may reduce the risk from heart failure and malignant arrhythmias in patients suffering from hypertension.

Conclusions:

Supported by VEGA grants 2/0167/15, 2/0076/16, SKS grant.

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