Attenuation of High-Salt Diet-Induced Renin–Angiotensin–Aldosterone System (RAAS) Activation and Endothelial Dysfunction by Omega-3 Fatty Acids and Quercetin Supplementation in Wistar Rats

Excessive dietary salt intake is a major contributor to hypertension and many other cardiovascular dysfunctions. The mechanism of actions usually involves; activation of the renin–angiotensin–aldosterone system (RAAS), increased oxidative stress, and impaired endothelial nitric oxide signaling.

This study investigated the effects of omega-3 fatty acids and Quercetin, individually and in combination, on biomarkers of RAAS activation, oxidative status, and endothelial function in high-salt diet-fed Wistar rats.

Thirty-Five (35) male Albino Wistar rats(180-220g) were randomly assigned into seven groups(n=5). Group 1 (Control ) received rat chow and water only, Group2 (Sham control-1)  received 1ml/kg bw of DMSO ,  Group 3(Sham control -2) received 0.1ml/kg bw of Olive oil, Group 4 (HSF) received 8%NaCl diet + 1% drinking water. Group 5 (HSF + Omega-3) and Group 6 (HSF + Quercetin) received 14.29mg/kg bw of Omega-3 and 20mg/kg bw of Quercetin plus HSF respectively. Group7 (HSF+Omega-3+Quercetin) received a combination of Omega-3 and Quercetin plus HSF. Olive oil and DMSO served as vehicles of administration for omega 3 fatty acids and Quercetin respectively. Administration was done once orally for 42days(6weeks).After 42 days, blood samples were collected and serum levels  of angiotensin11 (Ang.11)  angiotensin-converting enzyme (ACE), nitric oxide (NO), nitric oxide synthase (NOS), and total antioxidant capacity (TAC) were evaluated.

The results indicated no significant difference among the different control groups. For high salt diet (HSF) group; Ang 11, ACE were significantly (P< 0.05) decrease compared to control groups. While serum levels of NO, NOS and TAC were significantly (P< 0.05) decreased. Indicating RAAS activation, endothelial dysfunction, and oxidative stress. For Omega 3 and Quercetin Supplementation groups; serum levels of angiotensin 11 and ACE were significantly (P< 0.05) decreased while NO, NOS and TAC were significantly increased, suggesting ameliorative potential of these agents.

Interestingly, the combined group was more effective. These findings suggest that omega-3 fatty acids and Quercetin exert synergistic protective effects against salt-induced cardiovascular dysfunction via modulation of the RAAS–oxidative stress–nitric oxide axis.