Objective: To explore the effects of total flavonoids of Hippophae rhamnoides L. (TFH), quercetin (Que) and isorhamnetin (Isor) on the intracellular free calcium (Ca~ 2+ _ i) in vascular smooth muscle cells (VSMC) of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).Methods: Fluo 3-acetoxymethylester(Fluo-3/AM) was used to observe the effects of TFH (100mg/L) and its essential monomers, namely Que (10~ -4 mol/L) and Isor (10~ -4 mol/L) on changes of Ca~ 2+ _ i in cultured SHR and WKY VSMC (abbr. to Ca-SHR & Ca-WKY) following exposure to high K~+, norepinephrine (NE) and angiotensin Ⅱ(AngⅡ), and to compare with the effects of verapamil (Ver). Results: (1) TFH, Que and Isor had inhibitory effects on resting Ca-SHR (P<0.05), but had no significant effects on Ca-WKY (P>0.05). (2) High K~+ could increase Ca-SHR more significantly than Ca-WKY (P<0.05); TFH, Que and Isor could inhibit the elevation of Ca~ 2+ _ i induced by high K~+-depolarization, with the effects similar to that of Ver, and the effect on Ca-SHR was more significant than that on Ca-WKY (P<0.05). (3) NE and AngⅡcould increase Ca-SHR more significantly than Ca-WKY (P<0.05), TFH, Que and Isor had remarkably inhibitory effect on the elevation of Ca-SHR and Ca-WKY induced by NE or AngⅡ. (4) In the absence of extracellular Ca~ 2+ , TFH, Que and Isor also had certain inhibitory effect on Ca-SHR and Ca-WKY induced by NE, and the effect on the former was more significant than that on the latter(P<0.05). Conclusion: TFH, Que and Isor might decrease the levels of Ca~ 2+ _ i in VSMCs by blocking both voltage-dependent calcium channels (VDC) and receptor-operated calcium channels (ROC) in physiological or pathological state, which may be one of the important mechanisms of their hypotensive and protective effects on target organs in patients with hypertension. Objective: To explore the effects of total flavonoids of Hippophae rhamnoides L. (TFH), quercetin (Que) and isorhamnetin (Isor) on the intracellular free calcium (Ca~ 2+ _ i) in vascular smooth muscle cells (VSMC) of spontaneously Hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).Methods: Fluo 3-acetoxymethylester (Fluo-3/AM) was used to observe the effects of TFH (100mg/L) and its essential monomers, namely Que (10~ -4 mol/L) and Isor (10~ -4 mol/L) on changes of Ca~ 2+ _ i in cultured SHR and WKY VSMC (abbr. to Ca-SHR & Ca-WKY) following exposure to high K~ Results of (1) TFH, Que and Isor had inhibitory effects on resting Ca-SHR (P<0.05), but Had no significant effects on Ca-WKY (P>0.05). (2) High K~+ promoted Ca-SHR more significantly than Ca-WKY (P<0.05); TFH, Que and Isor could inhibit the elevation of Ca~ 2+ _ i induced by high K~+-depolarization, with the effect similar To that of Ver, and the effect on Ca-SHR was more significant than that on Ca-WKY (P<0.05). (3) NE and AngIIcould increase Ca-SHR more significantly than Ca-WKY (P<0.05), TFH , Que and Isor had remarkably inhibitory effect on the elevation of Ca-SHR and Ca-WKY induced by NE or AngII. (4) In the absence of extracellular Ca~ 2+ , TFH, Que and Isor also had certain inhibitory effect on Ca -SHR and Ca-WKY induced by NE, and the effect on the former was more significant than that on the latter (P<0.05). Conclusion: TFH, Que and Isor might decrease the levels of Ca~ 2+ _ i in VSMCs By blocking both voltage-dependent calcium channels (VDC) and receptor-operated calcium channels (ROC) in physiological or pathological state, which may be one of the important mechanisms of their hypotensive and protective effects on target organs in patients with hypertension.