INFLUENCE OF ANTIHYPERTENSIVE DRUGS AND ANTIOXIDANTS ON PLATELETS AND ENDOTHELIAL FUNCTIONS OF SALT-INDUCED HYPERTENSION IN SPRAGUE DAWLEY RATS
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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.
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.
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