CHROMAFFIN CELL-ACTION POTENTIALS AND THEIR POSSIBLE ROLE IN ADRENALINE SECRETION FROM RAT ADRENAL-MEDULLA
CHROMAFFIN CELL-ACTION POTENTIALS AND THEIR POSSIBLE ROLE IN ADRENALINE SECRETION FROM RAT ADRENAL-MEDULLA
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DOI：
10.1113/jphysiol.1980.sp013431
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发表时间：
1980-01-01
影响因子：
5.5
通讯作者：
RITCHIE, AK
中科院分区：
文献类型：
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作者：
KIDOKORO, Y;RITCHIE, AK
研究了大鼠肾上腺髓质动作电位在肾上腺素分泌中的作用。比较了不同处理对灌注肾上腺髓质的肾上腺素分泌的影响，以及类似处理对游离肾上腺染色质细胞尖峰频率的影响。KCl浓度在10 ~ 20 mM之间增加了分离的肾上腺染色质细胞的细胞外记录的尖峰频率。当KCl浓度为30mm时，在30mm -KCl的持续存在下，最初出现短暂的尖峰爆发，随后出现一段时间的不活动。河豚毒素（TTX, 6 .mu）M)降低了KCl诱发的峰值的幅度和频率。当KCl浓度为10和120 mM时，离体大鼠肾上腺素分泌速率增加，而KCl浓度为10 ~ 20 mM时，TTX能部分抑制肾上腺素分泌。在KCl浓度为30 mM或更高时，诱发分泌不再受TTX的影响。CoCl2 （5 mM）阻断了KCl峰值频率的增加，也阻断了所有浓度的KCl对肾上腺素分泌的刺激。四乙基氯化铵（10 mM）降低了穗频率，但大大延长了穗持续时间，增强了15 mM- kcl诱导的分泌。结果与以下解释一致。钾离子刺激肾上腺素分泌的TTX不敏感部分是由于钙离子通过电压依赖的钙离子通道流入，钙离子通道是钾离子稳态去极化的结果。分泌的TTX敏感部分表明，在KCl增强的尖峰活动期间，钙内流的额外增加。钙内流的增加可能通过电压依赖的钙通道发生，钙通道的激活是由尖峰中TTX敏感的Na组分引起的电压变化促进的，也可能通过Na通道本身发生。灌注肾上腺髓质中乙酰胆碱（ACh）的分泌刺激在15 .mu时为最大的一半。并在50 μ M左右开始饱和。当乙酰胆碱浓度为10 μ m时，TTX对其释放有部分抑制作用。小于等于M。讨论了动作电位在乙酰胆碱刺激肾上腺素释放中的可能作用。
The role of action potentials in adrenaline [epinephrine] secretion was investigated in the rat adrenal medulla. The effects of various treatments on adrenaline secretion from the perfused adrenal medulla were compared with the effects of similar treatments on spike frequency in dissociated adrenal chromaffin cells. KCl concentrations between 10 and 20 mM increased the extracellularly recorded spike frequency of dissociated adrenal chromaffin cells. Upon perfusion by a KCl concentration of 30 mM there was an initial brief burst of spikes followed by a period of inactivity in the continued presence of 30 mM-KCl. Tetrodotoxin (TTX, 6 .mu.M) decreased the amplitude and frequency of the KCl evoked spikes. The rate of adrenaline secretion from the isolated perfused rat adrenal gland increased as the KCl concentration was raised to 10 and up to 120 mM. Secretion which was evoked by KCl concentrations between 10 and 20 mM was partially inhibited by TTX. At KCl concentrations of 30 mM or greater evoked secretion was no longer affected by TTX. CoCl2 (5 mM) blocked KCl increase of spike frequency and also blocked stimulation of adrenaline secretion by all concentrations of KCl tested. Tetraethylammonium chloride (10 mM), which decreased spike frequency but greatly prolonged the spike duration, enhanced secretion induced by 15 mM-KCl. The results are consistant with the following interpretation. The TTX insensitive portion of the KCl-stimulated adrenaline secretion is due to Ca influx through voltage-dependent Ca channels which are open as a consequence of the steady-state level of KCl depolarization. The TTX sensitive portion of secretion is indicative of an extra increment of Ca influx during spike activity enhanced by KCl. This increment of Ca influx may occur through voltage-dependent Ca channels whose activation is facilitated by the voltage changes caused during the TTX sensitive Na component of the spike and possibly through the Na channel itself. Stimulation of secretion by acetylcholine (ACh) in the perfused adrenal medulla was half maximal at 15 .mu.M and began to saturate around 50 .mu.M. Release was partially inhibited by TTX only when the concentration of ACh was 10 .mu.M or less. The possible role of action potentials in ACh-stimulated adrenaline release is discussed.