Altered Potassium Ion Channel Function as a Possible Mechanism of Increased Blood Pressure in Rats Fed Thermally Oxidized Palm Oil Diets

ABSTRACT

Intake of thermally oxidized palm oil leads to cytotoxicity and alteration of the potassium ion channel function. This study investigated the effects of fresh and thermally oxidized palm oil diets on blood pressure and potassium ion channel function in blood pressure regulation. Male Wistar rats were randomly divided into three groups of eight rats. Control group received normal feed; fresh palm oil (FPO) and thermally oxidized palm oil (TPO) groups were fed a diet mixed with 15% (weight/weight) fresh palm oil and five times heated palm oil, respectively, for 16 weeks. Blood pressure was measured; blood samples, hearts, and aortas were collected for biochemical and histological analyses. Thermally oxidized palm oil significantly elevated basal mean arterial pressure (MAP). Glibenclamide (10⁻⁵ mmol/L) and tetraethylammonium (TEA; 10⁻³ mmol/L) significantly raised blood pressure in TPO compared with FPO and control groups. Levcromakalim (10⁻⁶ mmol/L) significantly (p < .01) reduced MAP by 32.0% in FPO and by 5.4% in TPO. NS1619 (10 mmol/L) significantly (p < .01) decreased MAP by 19.5% in FPO and by 8% in TPO. The TPO significantly (p < 0.01) increased the tissue levels of peroxide, total cholesterol, triglyceride, and low-density lipoprotein cholesterol while catalase and superoxide dismutase activities were significantly (p < .01) decreased compared with control and FPO groups. Histological alterations were prominent in aortas and hearts of rats in the TPO group. These results suggest that prolonged consumption of repeatedly heated palm oil increases MAP probably due to the attenuation of adenosine triphosphate–sensitive potassium (K_ATP) and large-conductance calcium-dependent potassium (BK_Ca) channels, tissue peroxidation, and altered histological structures of the heart and blood vessels.

KEYWORDS:

• aorta
• blood pressure
• dietary oils
• levcromakalim
• lipid profile
• tetraethylammonium-NS1619

Acknowledgments

The authors of this research study acknowledge the technical assistance of Dr. O. O. Okwari and Dr. Sikirullai Olatunde Jeje of the Department of Physiology, Cross River University of Technology, Calabar, Okuku Campus, Cross River State, Nigeria.

Declaration of interest

The authors declare no conflicts of interest. The authors alone are responsible for the content and writing of the article.

About the authors

E. E. Nkanu is a Ph.D. holder and a faculty member in the Department of Physiology, Cross River State University of Technology, Okuku Campus, Cross River State. He has research interest in cardiovascular physiology with bias on ion channels.

D. U. Owu has a Ph.D. in cardiovascular physiology and has a faculty position in Department of Physiology, University of Calabar, Calabar, Cross River State, Nigeria. He is a professor of Cardiovascular Physiology with special interest in plant products affecting blood pressure and cardiac function.

E. E. Osim is a Ph.D. holder and a professor of Physiology with special interest in gastrointestinal tract and neurophysiology. He is employed in the Department of Physiology, College of Medical Sciences of the University of Calabar, Calabar, Nigeria.