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首页> 外文期刊>Physiological Reports >Contributions of cardiac “funny” (f) channels and sarcoplasmic reticulum Ca2+ in regulating beating rate of mouse and guinea pig sinoatrial node
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Contributions of cardiac “funny” (f) channels and sarcoplasmic reticulum Ca2+ in regulating beating rate of mouse and guinea pig sinoatrial node

机译：心脏“滑稽”（f）通道和肌浆网Ca2 +在调节小鼠和豚鼠窦房结搏动率中的作用

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AbstractThe aim of this study was to investigate the effects on spontaneous beating rate of mouse atrial preparations following selective block of cardiac “funny” (f) channels, I(f), and/or suppression of sarcoplasmic reticulum (SR) function in the absence and presence of β-adrenoceptor stimulation. ZD7288 [to block I(f)] caused a substantial reduction (222 ± 13 bpm) in beating rate from 431 ± 14 to 209 ± 14 bpm, ryanodine alone (to block SR Ca2+ release) reduced beating rate by 105 ± 11 bpm, with subsequent addition of ZD7288 further reducing rate by 57 ± 9 bpm. Cyclopiazonic acid (CPA) alone (to inhibit Ca2+ reuptake by the SR) reduced beating rate by 148 ± 13 bpm with subsequent addition of ZD7288 further reducing rate by 79 ± 12 bpm. In additional experiments measuring Ca2+ transients in the SA node region using Rhod-2, effects of ivabradine and ZD7288 on rate were again substantially reduced after CPA. Effects of CPA alone on rate developed much more slowly than effects on Ca2+ transient amplitude. ZD7288, ivabradine, and CPA reduced the slope and maximum response of the log(concentration)–response curves for effects of isoprenaline on beating rate. Very little response to isoprenaline remained after treatment with CPA followed by ZD7288. Similar changes in isoprenaline log(concentration)–response curves were seen in guinea pig preparations. These observations are consistent with a role for Ca2+ released from the SR in regulating I(f) and therefore beating rate of SA node preparations; there appear to be additional contributions of SR-derived Ca2+ to effects of β-adrenoceptor stimulation on beating rate that are independent of I(f).
机译：摘要本研究旨在研究选择性阻断心脏“滑稽”（f）通道，I（f）和/或抑制肌浆网（SR）功能对小鼠心房制剂自发搏动率的影响。和β-肾上腺素受体刺激的存在。 ZD7288 [用于阻断I（f）]导致搏动速率从431±14 bpm大幅降低（222±13 bpm），仅使用丹参碱（以阻断SR Ca 2 + 释放）将跳动速率降低了105±11 bpm，随后添加ZD7288进一步降低了57±9 bpm。单独使用Cyclopiazonic acid（CPA）（以抑制SR吸收Ca 2 + 再摄取）将跳动率降低148±13 bpm，随后添加ZD7288则进一步降低了79±12 bpm。在使用Rhod-2测量SA结区域内Ca 2 + 瞬变的其他实验中，伊伐布雷定和ZD7288对速率的影响在CPA后再次显着降低。单独的CPA对速率的影响要比对Ca 2 + 瞬变幅度的影响慢得多。 ZD7288，伊伐布雷定和CPA降低了异丙肾上腺素对跳动速率的影响的log（浓度）-响应曲线的斜率和最大响应。 CPA继之以ZD7288治疗后，对异丙肾上腺素的反应极少。在豚鼠制剂中，异丙肾上腺素对数（浓度）-反应曲线的变化相似。这些观察结果与从SR释放的Ca 2 + 在调节I（f）从而调节SA结制备的跳动率中的作用是一致的。 SR衍生的Ca 2 + 对β-肾上腺素能受体刺激的搏动率的影响似乎与I（f）无关。

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