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ABSTRACT
High salt intake causes hypertension in both animals and in humans as well as elicit other deleterious effects in body organs. Antioxidative agents are reported to provide some cardiovascular protection, however their effect in ameliorating salt-induced deleterious effects has not been fully characterised. Thirty five Sprague Dawley male rats weighing between 250g and 300g were acquired and randomly separated into 7 groups of 5 rats each. Group 1: control; received normal rat chow and tap water ad libitum, Group 2: high salt diet of 8% NaCl (HS); group 3: HS + high magnesium sulphate (4mM)/day, group 4: HS + kolaviron (200mg/kg wt/day), group 5: HS + methylene blue (400mg/kg wt/day), group 6: HS + Lisinopril (2.3mg/kg wt/day) and group 7: HS + ascorbic acid. Feeding and drug administration were done for a period of 6 weeks. All drugs route of administration was by oral gavage according to body weight. 24 hours after the last administration, animals were sacrificed using chloroform. Carefully the heart, aorta, and mesenteric arteries were isolated for alpha and beta-myosin heavy chains (α-MHC),(β-MHC) expressions, oxidative stress markers, histological, and immunochemical assay. All data were analyzed using the GraphPad Prism, The results obtained showed increase in mean arterial blood pressure (MAP) in the salt-loaded rats and attenuation in MAP in the tests groups cotreated with antioxidative agents compared with the control. Oxidative markers (MDA, SOD, GPx and CAT) were significantly decreased in the heart and arterial blood vessels. β-MHC expressions were upregulated in the test groups compared with control in both myocardial cells and aorta and mesenteric arteries; whereas α-MHC expressions were moderately expressed in the test groups in the heart and aorta but down regulated in the mesenteric artery compared with control. Some structural changes in the heart and arterial blood vessels were observed in the histochemistry. In conclusion, high salt diet causes increase oxidative stress, hypertension and upregulation of β-MHC expressions in cardiac, aorta andmesenteric arterial blood vessels in the salt, and salt cotreated groups and down regulation of α-MHC expression in mesenteric artery compared with the control in Sprague-Dawley rats.
