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Background and objective: Curcumin exhibits cardiovascular protective effects regarding to its antioxidant and anti-inflammatory effects. This study hypothesized that curcumin would modulate vascular responses to sympathetic nerve stimulation in normotensive and hypertensive rats.
Methods: Male Sprague-Dawley rats (200-225 g) were induced hypertension by administering NG-nitro-L-arginin e methyl ester (L-NAME) (40 mg/kg/day, 3 weeks) in drinking water while normotensive rats were given distilled water. Mesenteric vascular beds from both normotensive and hypertensive rats were isolated. Chemical removal of vascular endothelium by sodium deoxycholate was performed and preparations were pretreated with capsaisin (0.1 µM), to deplete sensory neurotransmitters. Contractile responses to electrical field stimulation (EFS 5-40 Hz, 90V, 1 ms for 30s, at 5-min intervals) and exogenous noradrenaline (NA) (1 µmol-1 mmol) or phenylephrine (PE) (1 µmol-1 mmol) were examined in the presence of curcumin (10-6 M).
Results: Hypertensive rats showed high systolic blood pressure compared to normotensive rats (178±5 vs. 121±2 mmHg, p<0.001). Curcumin significantly attenuated sympathetic nerve mediated-responses (p<0.05, n=6,) and contractile responses to exogenous NA and PE in all preparations (p<0.05).
Conclusions: Curcumin exhibits an inhibitory effect on sympathetic neurogenic vasoconstrictor responses in normotensive and hypertensive rat mesenteric vascular beds. This inhibitory effect is likely to involve the postjunctional site inhibition.
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