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ABSTRACT
Experimental evidence suggests that high salt diet has been shown to alter immune cells function and inflammation responses whereas anti-hypertensives drugs are efficacious in management of hypertensive conditions, however, their effects and mechanisms of action on pro-inflammatory markers have not been fully characterized. This present study examined the effects of different antihypertensive drugs on inflammatory cytokines in salt-dependent pre-hypertensive animal model. Twenty-five (25) male Sprague-Dawley rats weighing between 100-130g were randomly divided into 5 groups of 5 rats each. Group A; Control rats received normal chow feed and tap water. Group B; received high salt diet of 8% NaCl (HSD) and tap water for 8 weeks. Groups C to E received HSD (+ Losartan 10mg+ Lisinopril 2.3mg + Verapamil 0.1mg) kg -1 body weight respectively by oral gavage for 8 weeks. Blood pressure (BP) (mmHg) and heart rate (bpm) measurement were done in conscious animal by curf tail artery before the animals were sacrificed using chloroform anaesthesia. 5ml of blood sample was collected for biochemical analysis. The results showed that Mean arterial blood pressure (MAP) significantly increased in salt-loaded rats compared with the control, whereas the antihypertensive drugs caused attenuation in blood pressure increase when compared with the salt-loaded group. Lisinopril in particular reversed this trend; suggesting renin angiotensin pathway to be the major pathway for salt loading to cause hypertension but there was no significant change in the heart rate of the animals. Neutrophil-to-lymphocyte ratio was significantly increased in salt-loaded rats compared with control and much more in Lisinopril and verapamil when compared with the salt-loaded group. Interleukin-6 was significantly increased in salt-loaded rats compared with control whereas there was no significant change when treated with lisinopril and losartan, but verapamil ameliorated its effects when compared with the salt-loaded group. TNF-A level was significantly increased in salt-loaded rats compared with control whereas the anti-hypertensives ameliorated this effect when compared with the salt-loaded group. ROS was significantly increased in salt-loaded rats compared with control whereas the increase in ROS level was attenuated in HSD-co treated with losartan and verapamil when compared with the salt treated group. In conclusion, this study shows that excessive high salt consumption triggers inflammatory tissue responses with implication of the immune system as crucial co-contributor to the development of hypertension and deleterious cellular effects. But lisinopril, losartan and verapamil could be useful therapeutically in ameliorating the adverse inflammatory effects.
