Komai H, Rusy B F
Department of Anesthesiology, University of Wisconsin, Madison 53792-3273.
Cardiovasc Res. 1993 May;27(5):801-6. doi: 10.1093/cvr/27.5.801.
The aim was to characterise the influence of a decrease in transsarcolemmal calcium influx on the calcium content of the sarcoplasmic reticulum and on the force of postrest contraction, which is largely activated by calcium released from the sarcoplasmic reticulum.
Isometric force of postrest contractions in isolated rabbit papillary muscles was measured in the absence and in the presence of ryanodine (1 microM). The force measured in the presence of ryanodine was used as an index of transsarcolemmal calcium influx. The calcium content of the sarcoplasmic reticulum was estimated by rapid cooling induced contracture measurements. Nickel (Ni2+) was used to decrease the calcium influx, and the results were compared to those obtained by lowering the extracellular calcium concentration.
The addition of Ni2+ or lowering extracellular Ca2+ markedly decreased the force of postrest contraction measured in the presence of ryanodine, and moderately decreased the force of postrest contraction measured in the absence of ryanodine. Neither the addition of Ni2+ nor lowering extracellular Ca2+ decreased maximum rapid cooling induced contracture; this was actually increased in the presence of Ni2+ even though a larger number of stimuli was required in the presence than in the absence of Ni2+ for the force of the subsequently elicited contracture to reach the maximum level.
The results suggest: (1) that a decrease in the calcium influx reduces the force of the postrest contraction by decreasing the amount of calcium required to trigger the release of calcium from the sarcoplasmic reticulum, without decreasing its maximum calcium content; and (2) that Ni2+ decreases the rate of filling of sarcoplasmic reticular calcium stores even though the calcium content of the sarcoplasmic reticulum after a sufficiently large number of beats is higher in the presence of Ni2+ than in its absence.
本研究旨在探讨肌膜钙内流减少对肌浆网钙含量以及静息后收缩力的影响,静息后收缩力主要由肌浆网释放的钙激活。
在离体兔乳头肌中,分别在无和有1 μM 兰尼碱的情况下测量静息后收缩的等长力。在有兰尼碱存在时测得的力用作肌膜钙内流的指标。通过快速冷却诱导挛缩测量来估算肌浆网的钙含量。使用镍(Ni2+)降低钙内流,并将结果与降低细胞外钙浓度所获得的结果进行比较。
添加Ni2+或降低细胞外Ca2+显著降低了在有兰尼碱存在时测得的静息后收缩力,并适度降低了在无兰尼碱存在时测得静息后收缩力。添加Ni2+和降低细胞外Ca2+均未降低最大快速冷却诱导挛缩;实际上,在有Ni2+存在时,最大快速冷却诱导挛缩增加,尽管与无Ni2+时相比,在有Ni2+存在时需要更多的刺激才能使随后引发的挛缩力达到最大水平。
结果表明:(1)钙内流减少通过减少触发肌浆网钙释放所需的钙量来降低静息后收缩力,而不降低其最大钙含量;(2)Ni2+降低肌浆网钙储存的充盈速率,尽管在有足够多次搏动后,有Ni2+存在时肌浆网的钙含量高于无Ni2+时。