ABSTRACT
Store-operated Ca(2+) entry (SOCE) has recently been proposed to contribute to Ca(2+) influx in vascular smooth muscle cells (VSMCs). Imperatorin is known for its potent vasodilatory effects as a dietary furanocoumarin. The study was designed to examine the hypothesis that SOCE have a functional role in imperatorin-induced vasodilation. Small mesenteric resistance arteries and mesenteric VSMCs were obtained from rats. Isometric tensions of isolated artery rings were measured by a sensitive myograph system. Laser scanning confocal microscopy was used to determine the intracellular Ca(2+) concentration of fluo-3-loaded VSMCs. Imperatorin (1-100 µM) relaxed artery rings precontracted by phenylephrine in a concentration-dependent manner. In cultured mesenteric VSMCs, passive store depletion by thapsigargin and active store depletion by phenylephrine both induced Ca(2+) influx due to SOCE. Imperatorin didn't inhibit SOCE-mediated increases in cytosolic Ca(2+) levels evoked by the emptying of the stores. In isolated artery rings, imperatorin didn't inhibit SOCE-induced contractions due to store depletion. Our results exclude SOCE mechanism of vasodilatation by imperatorin. But imperatorin is partly similar with nifedipine in vasorelaxation effect.
Subject(s)
Calcium/metabolism , Calcium/pharmacology , Furocoumarins/metabolism , Mesenteric Arteries/drug effects , Vasodilator Agents/metabolism , Aniline Compounds/metabolism , Animals , Calcium Channels/drug effects , Calcium Channels/metabolism , Calcium Channels/physiology , Calcium Signaling/drug effects , Furocoumarins/pharmacology , Ion Transport/drug effects , Male , Mesenteric Arteries/metabolism , Muscle, Smooth, Vascular/drug effects , Muscle, Smooth, Vascular/metabolism , Rats , Rats, Sprague-Dawley , Vasodilation/drug effects , Vasodilation/physiology , Vasodilator Agents/pharmacology , Xanthenes/metabolismABSTRACT
OBJECTIVE: To investigate the effects of Bai-Chuan capsule (BC) on the left ventricular hypertrophy in spontaneously hypertensive rats (SHR). METHODS: Taking SHR and Wistar Kyoto rats (WKY) as the model group and the control group respectively, Captopril as positive drug, administered BC 0.3 g/kg, Captopril 3.75 mg/kg or 0.5% CMC-Na to each group by ig for 3 months, and measured the change of blood pressure. The left ventricular mass index was calculated after rats were sacrificed. Left ventricle was used to pathological observations, plasma angiotensin II and aldosterone were measured by radioimmunoassay. CONCLUSION: BC can inhibit left ventricular hypertrophy, plasma level of angiotensin II and aldosterone to some extent in SHR.
