O. K. UCHE

High salt consumption is known to be detrimental to cardiovascular health and can lead to various problems. However, the effects of antihypertensive drugs and antioxidants on salt-induced vascular
dysfunction remain insufficiently explored. This study aimed to examine the influence of antihypertensive drugs and antioxidants on impact of salt-loading in platelet and endothelial function. Forty-eight male Sprague-Dawley rats were assigned to control group and different test groups receiving a high salt diet with different antihypertensive drugs and antioxidants interventions. The control group received a normal rat chow (0.3% NaCl) and water, the high salt (HS) group received rat chow containing (8% NaCl), others were fed on high salt diet (8% NaCl) with interventions including Lisinopril 2.3mg/kg/d, Losartan 0.1mg/kg/d, Verapamil 0.1mg/kg/d,m Vitamin C 100mg/kg/d, Magnesium 4.8mM and Kolaviron 200mg/kg/d. Drug administrations were by oral gavage. Blood pressure (mmHg) and heart rate (bpm) were monitored using the cufftail artery method. At the end of 8 weeks treatment period, animals were sacrificed using
chloroform anaesthesia, carefully, the abdominal cavity was cut open by mid-line incision using a clean dissecting set. Left ventricle, aorta and mesenteric artery were harvested and blood samples were collected for platelet count, platelet indices and gene protein expression analyses. The result showed a significant increase in the mean arterial pressure, systolic and diastolic pressure in saltloaded rats compared with control, the high salt + Lisinopril, Losartan, Verapamil, Vitamin C,
Magnesium and Kolaviron groups showed significant reduction in blood pressure compared with high salt group. There was a significant increase in platelet activating factor (PAF) gene expression
in high salt group compared with control. High salt co-treated with Lisinopril, Losartan, Verapamil, Vitamin C, Magnesium and Kolaviron groups showed significant decrease in PAF gene expression compared to high salt group. There were no significant changes in platelet count across groups compared with control. There was a significant decrease in mean platelet volume in HS + Lisinopril and HS + Verapamil groups compared with control but there were no significant changes in all the other groups compared with control. There were no significant changes in plateletcrit in all the groups compared with control. There were no significant changes in platelet distribution
width in all the groups compared with control. There was significant decrease in platelet large cell ratio in HS + Lisinopril, HS + Verapamil and HS + Kolaviron groups compared with control but
there were no significant changes in all the other groups compared with control respectively. In conclusion, this study provides evidence that suggests that high salt diet may alter platelets function through oxidative, and protein enzyme receptor pathways which may be explored for improvement in therapeutic interventions.

High salt consumption is known to be detrimental to cardiovascular health and can lead to various problems. However, the effects of antihypertensive drugs and antioxidants on salt-induced vascular dysfunction remain insufficiently explored. This study aimed to examine the influence of antihypertensive drugs and antioxidants on impact of salt-loading in platelet and endothelial function. Forty-eight male Sprague-Dawley rats were assigned to control group and different test groups receiving a high salt diet with different antihypertensive drugs and antioxidants
interventions. The control group received a normal rat chow (0.3% NaCl) and water, the high salt (HS) group received rat chow containing (8% NaCl), others were fed on high salt diet (8% NaCl) with interventions including Lisinopril 2.3mg/kg/d, Losartan 0.1mg/kg/d, Verapamil 0.1mg/kg/d, Vitamin C 100mg/kg/d, Magnesium 4.8mM and Kolaviron 200mg/kg/d. Drug administrations were by oral gavage. Blood pressure (mmHg) and heart rate (bpm) were monitored using the cufftail artery method. At the end of 8 weeks treatment period, animals were sacrificed using chloroform anaesthesia, carefully, the abdominal cavity was cut open by mid-line incision using a clean dissecting set. Left ventricle, aorta and mesenteric artery were harvested and blood samples were collected for platelet count, platelet indices and gene protein expression analyses. The result showed a significant increase in the mean arterial pressure, systolic and diastolic pressure in saltloaded rats compared with control, the high salt + Lisinopril, Losartan, Verapamil, Vitamin C, Magnesium and Kolaviron groups showed significant reduction in blood pressure compared with high salt group. There was a significant increase in platelet activating factor (PAF) gene expression in high salt group compared with control. High salt co-treated with Lisinopril, Losartan, Verapamil,
Vitamin C, Magnesium and Kolaviron groups showed significant decrease in PAF gene expression compared to high salt group. There were no significant changes in platelet count across groups compared with control. There was a significant decrease in mean platelet volume in HS +
Lisinopril and HS + Verapamil groups compared with control but there were no significant changes in all the other groups compared with control. There were no significant changes in plateletcrit in all the groups compared with control. There were no significant changes in platelet distribution width in all the groups compared with control. There was significant decrease in platelet large cell
ratio in HS + Lisinopril, HS + Verapamil and HS + Kolaviron groups compared with control but there were no significant changes in all the other groups compared with control respectively. In conclusion, this study provides evidence that suggests that high salt diet may alter platelets
function through oxidative, and protein enzyme receptor pathways which may be explored for improvement in therapeutic interventions.

High blood pressure is a mounting worldwide health crisis, and a diet consistently high in salt is a major contributor. Whereas, widespread use of silver nanoparticles (AgNPs) leads to bioaccumulation, with studies confirming their tendencies to induce toxicological effects in these same organs. The aim of this study was to compare the effects of some of the antihypertensive drugs, Amlodipine, Lisinopril, Ascorbic Acid, and Losartan, alongside Nanosilver on both the kidney and the brain function in rats fed a long-term high-salt diet. Sixty-four (64) male Sprague dawley rats where divided into 8 groups (8 rats per group). Group 1(control) was given normal rats chow and water, Group 2 received high salt diet containing 8% NaCl, Group 3 received Nano-sliver and normal feed, Group 4 received high salt diets and Nanosilver, Group 5, received Nanos liver and Amlodipine (1mg/kg body weight), Group 6 received high salt diet and Lisinopril (2.3mg/kg body weight/ day). Group 7 received high salt diet and Vitamin C (50mg/kg bw/ day). Group 8 received high salt diet and Losartan (10mg/kg bw/day) for 12 weeks. All the animals were allowed access to water ad libitum and drugs administered by oral gavage. The Neurobehavioral functions and cognitions were assessed using Open field apparatus for Novel object recognition test (NOR), Y-maze for spontaneous movement and elevated plus maze for anxiety levels. Statistical analysis was done using T- test Graph Pad Prism Version 10.2.2, with significance set at (P<0.05). At the end of the study, blood samples were collected for biochemical analysis for urea, creatinine, sodium, potassium and nitrogen ion. The results of the study demonstrated that while chronic high salt intake did not promote a significant long-term weight gain, it did not produce detectable in blood serum urea, creatinine, potassium and nitrogen ion. In conclusion, the present study showed no indication of dysfunction in the blood parameters examined. This gives confidence in the blood and renal safety profile.