Methyl Palmitate, a Potent Angiotensin Converting Enzyme Inhibitor, Attenuates Vascular Remodeling in L-NG-Nitro Arginine Methyl Ester-Induced Hypertensive Wistar Rat Models.

UNLABELLED: <p>

Introduction

Angiotensin converting enzyme (ACE) regulates blood pressure via the renin-angiotensin and bradykinin systems. Though synthetic ACE inhibitors are more effective, they pose several side effects. Methyl palmitate (MP), a natural fatty acid methyl ester with cytoprotective, antioxidant, anti-inflammatory, and vasodilatory properties, is not explored for its ACE inhibitory or antihypertensive potential. This study aimed to investigate the in vitro ACE inhibition of MP and its effect on L-NG-Nitro Arginine Methyl Ester (<sc>L</sc>-NAME)-induced hypertensive male Wistar rats.

METHODS

An in vitro ACE inhibition assay was conducted to compare the inhibition potency of MP with that of lisinopril. Male Wistar rats (n = 35, 7 per group) were grouped into control, disease control, and treatment groups receiving 100, 150, or 200 mg/kg/day of MP for 21 days each. Blood pressure, serum ACE activity, malondialdehyde (MDA), and nitric oxide (NO) levels in kidney tissue homogenate, and thoracic aorta histopathology were assessed.

RESULTS

MP inhibited ACE by 61.05% at 5 µ<sc>m</sc>, exceeding lisinopril's 41.67%. High-dose MP significantly reduced serum ACE and MDA levels, while increasing NO (p < 0.001). Histopathology revealed near-normal vasculature, although changes in blood pressure were not statistically significant (p > 0.05).

CONCLUSION

MP demonstrates strong natural ACE inhibition, antioxidant, and vascular protective effects, supporting further research for therapeutic optimization. </p>.