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首页> 外文期刊>Life sciences >Functional role of ryanodine-sensitive Ca2+ stores in acidic pH-induced contraction in Wistar Kyoto rat aorta.
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Functional role of ryanodine-sensitive Ca2+ stores in acidic pH-induced contraction in Wistar Kyoto rat aorta.

机译：ryanodine敏感的Ca2 +存储在Wistar Kyoto大鼠主动脉的酸性pH诱导的收缩中的功能作用。

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Acidic pH induced a contraction in the isolated aorta from Wistar Kyoto rat. The magnitude of contraction was dependent upon the degree of extracellular acidification. The maximum level of contraction observed at pH 6.5 was 84.6 +/- 3.4% of the 64.8 mM KCl-induced contraction. To investigate the role of extracellular as well as intracellular Ca(2+) in acidic pH-induced contraction (APIC), we changed the extracellular pH in the presence of EGTA. Sustained contraction induced by acidic pH in the presence of extracellular Ca(2+) was completely abolished in the presence of EGTA, while a transient but significant contraction was still observed. Ryanodine, a selective ryanodine receptor blocker and cyclopiazonic acid (CPA), an inhibitor of sarco-/endoplasmic reticulum Ca(2+) ATPase, abolished the transient contraction, when pH was decreased in Ca(2+)-free solution. On the other hand, neither xestospongin C, a selective inositol-1,4,5-trisphosphate receptor antagonist nor U-73122, a phospholipase C inhibitor showed this effect. These results suggest the involvement of Ca(2+) release from ryanodine-/CPA-sensitive store of sarcoplasmic reticulum (SR). In normal Ca(2+)-containing solution, ryanodine and CPA did not alter the maximum level of APIC. However, they significantly decreased the rate of rise of APIC. U-73122, suppressed the maximum contraction induced by acidic pH without affecting the rate of rise of APIC, while xestospongin C and U-73343, an inactive analogue of U-73122, had no effect on both parameters of APIC. From these results, it is concluded that acidic pH induces Ca(2+) release from the ryanodine-/CPA-sensitive store of SR and that release provides supportive effect on initiating rapid transient contraction, but not on the sustained contraction, which is entirely due to Ca(2+) influx.
机译：酸性pH诱导Wistar Kyoto大鼠分离的主动脉收缩。收缩的程度取决于细胞外酸化的程度。在pH 6.5时观察到的最大收缩水平是64.8 mM KCl诱导的收缩的84.6 +/- 3.4％。若要调查细胞外以及细胞内Ca（2+）在酸性pH诱导的收缩（APIC）中的作用，我们在存在EGTA的情况下更改了细胞外pH。在存在EGTA的情况下，在细胞外Ca（2+）存在下由酸性pH诱导的持续收缩被完全消除，而仍然观察到短暂但明显的收缩。 Ryanodine，选择性的ryanodine受体阻滞剂和环吡嗪酸（CPA），肌浆/内质网Ca（2+）ATPase的抑制剂，取消了瞬时收缩，当无Ca（2+）溶液中的pH降低时。另一方面，选择性的肌醇-1,4,5-三磷酸受体拮抗剂西雌皂苷C和磷脂酶C抑制剂U-73122均未显示这种效果。这些结果表明，Ca（2+）释放从肌浆网（SR）的ryanodine- / CPA敏感存储。在正常的含Ca（2+）的溶液中，ryanodine和CPA不会改变APIC的最大水平。但是，它们大大降低了APIC的增长率。 U-73122抑制了酸性pH诱导的最大收缩，而没有影响APIC的上升速率，而异源皂苷C和U-73343（U-73122的非活性类似物）对APIC的两个参数均没有影响。从这些结果可以得出结论，酸性pH诱导SR的对ryanodine / CPA敏感的存储区释放Ca（2+），并且该释放对启动快速瞬态收缩提供支持作用，但对持续收缩却不提供支持作用，这完全是完全的由于Ca（2+）涌入。

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