Proceedings of The Physiological Society
University of Oxford (2011) Proc Physiol Soc 23, PC104
Curcumin decreased vascular responses to sympathetic nerve stimulation in the mesenteric vascular bed of normotensive and hypertensive rats
P. Pakdeechote1, U. Kukongviriyapan1, W. Berkban1, P. Prachaney2, P. Tangsucjarit3, V. Kukongviriyapan3
1. Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 2. Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. 3. Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Curcumin is a major active compound derived from the spice turmeric. Previous studies have shown that curcumin exhibits a cardiovascular protective effect, however, little is known with regard to its effect on a vascular dysfunction in a hypertensive condition. We hypothesized that curcumin modulates vascular responses to sympathetic nerve stimulation in normotensive and hypertensive rats. Male Sprague-Dawley rats (220-225 g) were induced hypertension by administering NG-nitro-L-arginine methyl ester (L-NAME) (50 mg/kg/day, 3 weeks) in drinking water while normotensive rats were given distilled water. Rats with systolic blood pressure (SBP) higher than 160 mmHg (tail cuff measurement) were considered to be hypertension. They were anesthetized with sodium pentobarbital (50 mg/kg, i.p.) followed by exsanguinations. Mesenteric vascular beds from both normotensive and hypertensive rats were isolated and set up for perfusion (1). After chemical removal of vascular endothelium by sodium deoxycholate (1.8 mg/ml, 30s), preparations were pretreated with capsaisin (10-7 M) to deplete sensory neurotransmitters and to desensitize vanilloid receptors (2). Contractile responses to electrical field stimulation (EFS 5-40 Hz, 90V, 1 ms for 30s, at 5-min intervals) were performed. A second frequency response curve was generated after a further 30 minutes and served as a time control. Effects of curcumin (10-6 M) on sympathetic nerve mediated vasoconstriction were tested. Dose-dependent contractile responses to exogenous noradrenaline (NA) (1 µmol-1 mmol) or phenylephrine (PE) (1 µmol-1 mmol) were examined. L-NAME induced-hypertensive rats showed higher SBP compared to normotensive rats (178±5 vs. 121±2 mmHg, p<0.001, n=21, unpaired t-test). Perfusion pressure of hypertensive preparations was significantly higher than that of normotensive preparations (37±2 vs. 26±2 mmHg, p<0.05, n=21, unpaired t-test). Curcumin significantly attenuated sympathetic nerve mediated-responses (p<0.05, n=6, ANOVA) and contractile responses to exogenous NA and PE in all preparations (p<0.05, n=6, ANOVA). We have shown that curcumin exhibits an inhibitory effect on sympathetic neurogenic vasoconstrictor responses in normotensive and hypertensive rat mesenteric vascular beds and it may not have direct effect on the availability of NA. This inhibitory effect is likely to involve the postjunctional site inhibition. Thus, the direct effect of curcumin on vascular responses and the underlying mechanisms need to be evaluated in the rat perfused mesenteric vascular bed under raised tone conditions.
Where applicable, experiments conform with Society ethical requirements