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Abstract
immune markers and antihypertensive drugs. Despite knowing the detrimental effects of salt on blood pressure, the specific molecular mechanisms connecting these factors are not fully understood and how antihypertensive drugs affect immune function markers. The aim of this study is to see how antihypertensive medications affect immune function markers in a salt-loaded animal model. Twenty-five Sprague Dawley male rats weighing between 110g-130g was purchased from Lagos and housed in the Animal Unit of the Department of Pharmacology, and allowed to acclimatize for 2 weeks thereafter were randomly divided into 5 groups of 5 rats each. Group 1; control received normal rat chow and tap water, Group 2; Received high salt diet of 8% NaC1 (HS) alone for 8 weeks as described by, Group 3; Received high salt diet + 2.3mg/kg/d Lisinopril, Group 4; Received high salt + 0.1mg/kg/d verapamil, Group 5; Received high salt + 10mg/kg/d Losartan. Feeding and drug administration was by oral gavage for 8 weeks. Blood pressure (BP) (mmHg), heart rate (bpm) and weight measurement was done before theNanimals were humanely sacrificed using chloroform anaesthesia. The result shows a significant increase in the Mean arterial blood pressure in salt-loaded rats compared with the control, while antihypertensive drugs caused attenuation in blood pressure increase when compared with the salt-loaded group. Lisinopril in particular reversed the trend; suggesting renin angiotensin-mediated primary pathway in salt-induced hypertension. There were no significant changes in the heart rate of the animals. Neutrophil-to-lymphocyte ration was significantly increased in salt-loaded rats compared with control and much more in Lisinopril and verapamil co-treated salt-loaded rats. The result shows a significant increase in the salt loaded group when compared with the control group, meanwhile there was no significant difference in the salt loaded group treated with different antihypertensive drugs lisinopril and losartan compared with the salt loaded while verapamil shows a significant decrease in interleukin-6 levels when compared with the high salt group. Tumor necrosis factor (TNF-α) significantly increased in salt-loaded rats compared with the control, while in antihypertensive drugs it shows a decrease when compared with the salt-loaded group. Reactive oxygen species (ROS) significantly increased in salt-loaded rats compared with the control; in lisinopril it shows no significant difference when compared with the salt-loaded group while lorsartan and verapamil shows a decrease in ROS activities. In conclusion, this research shows that excessive high salt consumption triggers inflammatory tissue responses which could lead to hypertension and this project study is a pointer to the fact that increases activity of immune cells could pre dispose to hypertension and this effect are ameliorated by antihypertensive drugs, especially lisinopril and verapamil.
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