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应用双波长微荧光检测技术研究血管紧张素瞬间及持续刺激对乳鼠培养心肌细胞内游离钙的影响。结果显示,当加入血管紧张素Ⅱ（Ang Ⅱ）（10~(-10)mol/L）时,可观察到一个瞬间上升波峰,继而恢复,钙搏动振幅及频率无明显改变。加入Ang Ⅱ（10~(-8)mol/L）时,出现一个较为陡直的上升支,且有钙搏动频率加快,振幅增大。当Ang Ⅱ的加入量增至10~(-6)mol/L时,舒张期胞内钙浓度[Ca~(2+)]i明显增高达374.6±8.2nmol/L,与给药前95.7±8.4nmol/L比较差异有极显著性（P<0.01）,并呈现约几十秒钟的Ca~(2+)静止期。说明Ang Ⅱ可诱发胞内钙浓度的瞬间增高,且随剂量的不同表现为正性肌力和负性肌力两种作用。Ang Ⅱ对胞内钙的影响可被选择性的AT_1受体亚型拮抗剂DuP753所消除,但Ang Ⅱ受体亚型拮抗剂PD123319对Ang Ⅱ的作用无影响。阻滞电压依赖性Ca~(2+)通道可降低胞内钙浓度,但仅能部分地减少Ang Ⅱ对Ca~(2+)的影响。内质网Ca~(2+)-ATP酶抑制剂thapsigargin可降低或消除Ca~(2+)对Ang Ⅱ的反应,因此,Ang Ⅱ瞬间刺激所诱发的胞内游离Ca~(2+)的变化主要取决于内质网的Ca~(2+)释放。Ang Ⅱ和AngⅠ持续刺激均能使心肌细胞内Ca~(2+)升高,且随时间延长而递增。AngⅡ受体拮抗剂和转换酶抑制剂可消除或减弱二者的作用。说明心肌?
Dual-wavelength micro-fluorescence detection technique was used to study the effects of transient and continuous stimulation of angiotensin on intracellular free calcium in cultured neonatal rat cardiomyocytes. The results showed that when adding Ang Ⅱ (10 ~ (-10) mol / L), an instantaneous rising peak was observed, and then recovered. The amplitude and frequency of calcium pulsation did not change significantly. When Ang Ⅱ (10 ~ (-8) mol / L) was added, a steeper steepening branch appeared, and the frequency of calcium pulsation accelerated and the amplitude increased. When the amount of Ang Ⅱ increased to 10 -6 mol / L, the intracellular diastolic calcium concentration [Ca 2+] i increased significantly to 374.6 ± 8.2 nmol / L, compared with 95.7 ± The difference of 8.4nmol / L was significant (P <0.01), and showed a Ca ~ (2 +) quiescent period of about tens of seconds. Ang Ⅱ induced intracellular calcium concentration can be transiently increased, and with the different doses of positive and negative muscle strength of the two performance. The effect of Ang Ⅱ on intracellular calcium can be abolished by the selective AT1 receptor subtype antagonist DuP753, but Ang Ⅱ receptor subtype antagonist PD123319 has no effect on Ang Ⅱ. Blocking the voltage-dependent Ca 2+ channel decreased intracellular calcium concentration, but only partially reduced the effect of Ang Ⅱ on Ca 2+. Endoplasmic reticulum Ca ~ (2 +) - ATPase inhibitor thapsigargin can reduce or eliminate the reaction of Ca ~ (2+) to Ang Ⅱ. Therefore, the intracellular free Ca ~ (2+) The changes mainly depend on the Ca ~ (2+) release from the endoplasmic reticulum. Continuous stimulation with Ang Ⅱ and Ang Ⅰ could increase Ca 2+ in myocardial cells and increase with time. Ang II receptor antagonists and converting enzyme inhibitors can both eliminate and attenuate their effects. Explain the heart?