红曲降血压的血管机制:抑制平滑肌钙通道并激发其一氧化氮释放

THE VASCULAR MECHANISM OF MONASCUS HYPOTENSIVE EFFECT: BLOCK CALCIUM CHANNEL AND INCREASE NITROGEN OXIDE PRODUCTION OF SMOOTH MUSCLE

目的:探讨红曲的降血压机制。方法和结果:在离体血管环,去甲肾上腺素(NE)预刺激使血管收缩后加入红曲5mg/ml可明显舒张血管,舒张百分比为(70.84±14.74)%。这一舒张血管作用与血管内皮完整度无关。加入吲哚美辛(Indo),阻断前列腺环素(PGI)生成,对红曲的舒张血管作用没有影响(P>0.05)。而加入左旋硝基精氨酸(L-NNA)阻断平滑肌细胞的NO合成,则可明显抑制红曲的舒张血管作用(P<0.05)。红曲可使CaCl2、KCl和NE量效曲线均明显右移(P<0.05),表明红曲可抑制细胞膜钙通道,包括电位调控性钙通道(VOC)和受体调控性钙通道(ROC)。NE收缩血管反应中Ca2+来自细胞内和细胞外,红曲对细胞内钙引起的收缩没有影响,但可明显抑制细胞外钙引起的收缩。结论:红曲可通过刺激平滑肌细胞产生NO和抑制钙通道而引起血管舒张,这可能是其降血压的主要血管机制。

Objectives： The hypotensive effect of monascus was studied by rat aortic rings in vitro. Method and Results： The distinct relaxation of monascus was obviously reduced in the presence of precontraction which was caused by N^G-nitro-L-arginine （L-NNA, 1 × 10^4mol/L）, while indomethacin （1 × 10^6mol/L） did not affect the tension of the aortic rings. These results showed that monascus could relax aortic rings contracted with or without endothelium by NE （3.0×10^7 mol/L） and the relaxation percentage was （70.84±14.74）%. The monascus-induced relaxation was induced by increasing the production of NO in smooth muscle, and was not related to endothelium of rat aortic rings. By adding monascus in advance, the cumulative concentration-response curves of rat aortic rings were shifted downwards by CaCl2, KCl and NE. These results showed that monascus could block the inward flow of calcium by voltage operative channel （VOC） and receptor operative channel （ROC）. Monascus had a repressive effect on the contraction induced by extracellular calcium, but not by intracellular calcium in aortic rings, while NE caused contraction by both extracellular and intracellular caleium. Conclusion： Monascus could induce relaxation of aortic rings by increasing NO in smooth muscle and blocking inward flow of calcium. That was probably the main vascular mechanism of its hypotensive effect.