Chrysin pretreatment improves mitochondrial enzymes and angiotensin converting enzymes in L-NAME induced hypertensive rats

Hypertension is one among the important factors that causes cardiovascular disorders. N^ùnitro-L-arginine methyl ester (L-NAME) induces hypertension by blocking nitric oxide (NO) synthesis. Aim of present study was to investigate the effects of chrysin is one of major flavnoids, on L-NAME-induced hypertensive rats. Induces hypertension in adult male wistar rats weighing 180–220 g by oral treated of L-NAME (40 mg/kg/day) dissolved in drinking water daily for 8 weeks. Experimental rats were oral treated with chrysin (25 mg/kg b.w). Both the systolic and diastolic blood pressure of control and experimental rats were measured by tail cuff plethysmography system.

In our studies results showed an increase in the levels of systolic and diastolic blood pressure, heart, liver, kidney, body weight, plasma, and aortic Angiotension converting enzymes (ACE), Sodium (Na⁺), Chloride (Cl⁻) levels in L-NAME treated rats. At the same time in L-NAME treated rats, there was a decrease in the levels of potassium (K⁺), Plasma and heart-aortic nitrite/nitrate level, mitochondrial enzymes in liver such as Isocitrate dehydrogenase (ICDH), áketoglutarate dehydrogenase (á-KGDH), Succinate dehydrogenase (SDH) and Malate dehydrogenase (MDH). Chrysin treatment prevented the increase in systolic and diastolic blood pressure in the L-NAME-treated rats. Blood pressure (BP) reduction was interrelated with a reduction in Na⁺, Cl⁻, ACE activity and increased K⁺, plasma and heart, aortic nitrite/nitrate levels. In contrast, L-NAME had opposite effects on mitochondrial liver enzymes, electrolytes, ACE and NO by treatment of chrysin.

Hence, the present findings might suggest that chrysin improve the balance between circulating nitric oxide and rennin-angiotensin system and beneficial effects on cardiovascular tissue through its ACE inhibitor activity.