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ABSTRACT
Despite imperial evidence on the effects of high salt consumption on blood pressure and its deleterious effects on several organs of the body, the specific molecular mechanism of salt-induced hypertension and possible ameliorative pharmacological and non pharmacological therapeutic and preventive protocols have not been fully elucidated. This study is aimed at examining the effect of salt-loading and comparative ameliorative effect of antioxidants on Nitric oxide in animal model of salt-induced hypertension, Thirty Sprague-Dawley male rats weighing between 90-110g were acquired and divided into 6 groups of 5 rats each after 2 weeks of acclimatization. Group 1: Control, received Standard diet rat chow and tap water ad libitum, Group 2 received high salt diet of 8% to induce hypertension, Group 3 received high salt diet and (2.3 mg/kg bwt/day) of lisinopril (LP) by oral means, Group 4 received high salt diet (HSD) and administered vitamin C (100mg/kg bwt/day), Group 5 received high salt diet (HSD) and High magnesium (4.8mM/day), Group 6 received high salt diet (HSD) and Kolaviron. Feeding and drug administration were by oral gavage for 8 weeks. Blood pressure (BP) (mmHg), heart rate (bpm) and weight measurement were done before the animals were humanely sacrificed using chloroform anaesthesia and 5ml of blood collected for biochemical analyses. The result showed a significant increase in the Mean arterial blood pressure (MAP) mmHg, the systolic and diastolic blood pressure in salt-loaded rats compared with the control, while the different antioxidants caused attenuation in blood pressure increase when compared with the high-salt diet group. There was no significant changes of the Heart rate in high salt diet groups treated with the antioxidants.Nitric-oxide (NO) level significant decreased in high salt diet group when compared with the control. The pattern remained the same in the HSD-groups co-treated with different antioxidants. In conclusion, the present study showed that high salt consumption causes decrease in endothelium nitric oxide production and plasma level which was not ameliorated by treatment with different antioxidants; suggesting that decrease in nitric oxide bioavailability as a mechanistic pathway for salt-induced hypertension.
