无机磷酸盐可降低皂素处理的大鼠心脏小梁肌浆网中的钙离子含量。
Inorganic phosphate decreases the Ca2+ content of the sarcoplasmic reticulum in saponin-treated rat cardiac trabeculae.
作者信息
Smith G L, Steele D S
机构信息
Institute of Physiology, University of Glasgow.
出版信息
J Physiol. 1992 Dec;458:457-73. doi: 10.1113/jphysiol.1992.sp019427.
Abstract
- Measurements of [Ca2+] were made in saponin-permeabilized rat ventricular trabeculae using the fluorescent indicator Indo-1. Application of caffeine (20 mM) caused a transient rise in [Ca2+] within the preparation as a result of Ca2+ release from the sarcoplasmic reticulum (SR). The size of the caffeine-induced Ca2+ transient was related to the amount of Ca2+ accumulated by the SR prior to addition of caffeine. Caffeine-induced Ca2+ release was abolished by ryanodine (10 microM), an inhibitor of SR Ca2+ release. 2. At a bathing [Ca2+] of 0.2 microM, the amount of Ca2+ released from the SR on addition of caffeine was sufficient to generate a tension transient. Ca2+ and tension responses were stabilized by application of caffeine at regular intervals (2 min). Addition of 10 mM inorganic phosphate (Pi) induced a transient increase in [Ca2+] within the preparation due to a net release of Ca2+ from the SR. The amplitude of subsequent caffeine-induced Ca2+ transients were reduced to 65 +/- 7.5% (mean +/- S.D., n = 13) of control. In addition, the accompanying tension transient fell to 45 +/- 6.9% of control. Removal of Pi caused a transient decrease in the [Ca2+] within the preparation consistent with a net increase in Ca2+ uptake by the SR. Subsequent caffeine-induced Ca2+ and tension transients returned to control levels. 3. Inclusion of Pi (2-30 mM) in the perfusing solution decreased the size of caffeine-induced Ca2+ and tension transients in a dose-dependent manner. 4. Addition of 10 mM ADP caused a transient increase in [Ca2+] and depressed subsequent caffeine-induced Ca2+ transients to a greater extent than 10 mM Pi. Despite the reduction in Ca2+ release from the SR, tension responses were larger in the presence of 10 mM ADP than under control conditions. This is a consequence of an increase in Ca(2+)-activated force by ADP. 5. A decrease in the amplitude of caffeine-induced Ca2+ transients also occurred on changing from a solution containing 1 mM ADP and 10 mM Pi to a solution with 10 mM ADP and 1 mM Pi. This confirms the previous observation that ADP is more effective than Pi at reducing caffeine-induced Ca2+ released from the SR. 6. Spontaneous oscillations of [Ca2+] and tension occurred in the presence of 0.5 microM Ca2+.(ABSTRACT TRUNCATED AT 400 WORDS)
摘要
- 使用荧光指示剂 Indo-1 在皂素通透的大鼠心室肌小梁中测量 [Ca2+]。施加咖啡因（20 mM）会导致制剂中 [Ca2+] 短暂升高，这是由于肌浆网（SR）释放 Ca2+ 所致。咖啡因诱导的 Ca2+ 瞬变大小与添加咖啡因之前 SR 积累的 Ca2+ 量有关。SR Ca2+ 释放抑制剂钌红（10 microM）可消除咖啡因诱导的 Ca2+ 释放。2. 在 0.2 microM 的浴液 [Ca2+] 条件下，添加咖啡因时从 SR 释放的 Ca2+ 量足以产生张力瞬变。通过定期（2 分钟）施加咖啡因可使 Ca2+ 和张力反应稳定。添加 10 mM 无机磷酸盐（Pi）会导致制剂中 [Ca2+] 短暂增加，这是由于 Ca2+ 从 SR 净释放所致。随后咖啡因诱导的 Ca2+ 瞬变幅度降至对照的 65±7.5%（平均值±标准差，n = 13）。此外，伴随的张力瞬变降至对照的 45±6.9%。去除 Pi 会导致制剂中 [Ca2+] 短暂下降，这与 SR 对 Ca2+ 摄取的净增加一致。随后咖啡因诱导的 Ca2+ 和张力瞬变恢复到对照水平。3. 在灌注液中加入 Pi（2 - 30 mM）会以剂量依赖性方式降低咖啡因诱导的 Ca2+ 和张力瞬变的大小。4. 添加 10 mM ADP 会导致 [Ca2+] 短暂增加，并比 10 mM Pi 更显著地抑制随后咖啡因诱导的 Ca2+ 瞬变。尽管 SR 释放的 Ca2+ 减少，但在 10 mM ADP 存在下张力反应比对照条件下更大。这是由于 ADP 增加了 Ca(2+) 激活的力。5. 从含有 1 mM ADP 和 10 mM Pi 的溶液变为含有 10 mM ADP 和 1 mM Pi 的溶液时，咖啡因诱导的 Ca2+ 瞬变幅度也会降低。这证实了先前的观察结果，即 ADP 在减少 SR 释放的咖啡因诱导的 Ca2+ 方面比 Pi 更有效。6. 在 0.5 microM Ca2+ 存在下会发生 [Ca2+] 和张力的自发振荡。（摘要截断于 400 字）
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