POSSIBLE ROLE OF A BETA-ADRENOCEPTOR IN REGULATION OF NORADRENALINE RELEASE BY NERVE-STIMULATION THROUGH A POSITIVE FEEDBACK MECHANISM
POSSIBLE ROLE OF A BETA-ADRENOCEPTOR IN REGULATION OF NORADRENALINE RELEASE BY NERVE-STIMULATION THROUGH A POSITIVE FEEDBACK MECHANISM
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DOI：
10.1111/j.1476-5381.1975.tb07328.x
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发表时间：
1975-01-01
影响因子：
7.3
通讯作者：
LANGER, SZ
中科院分区：
文献类型：
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作者：
ADLERGRASCHINSK.E;LANGER, SZ
1研究异丙肾上腺素、心得安和酚妥拉明对刺激节后神经诱发豚鼠心房去甲肾上腺素溢出的影响。2异丙肾上腺素(1.2倍10-8M)增加，而心得安(1.0倍10-7M)减少刺激神经刺激引起的去甲肾上腺素的溢出。这些效应小于酚妥拉明(3.1倍10-6M)，后者增加了神经刺激引起的[~3H]-去甲肾上腺素溢出量的大约三倍。3异丙肾上腺素、心得安和酚妥拉明对去甲肾上腺素在豚鼠心房的蓄积无明显影响。4异丙肾上腺素(1.2倍10-8M)的正性变时性效应约为最大值的80%。另一方面，心得安使豚鼠心房对神经刺激的频率反应曲线和对外源性去甲肾上腺素的浓度反应曲线右移。5普奈洛尔不改变猫的点滴膜对神经刺激的频率反应曲线，而3.9倍10-负6M的N，-2-(2，6-二甲基苯氧基)丙基-N，N，N-三甲基铵(β-甲基-TM10)使频率-反应曲线右移，斜率下降。心得安和β-甲基-TM10均不影响对外源性去甲肾上腺素的反应。6.异丙肾上腺素和心得安对递质释放的影响与以下观点是一致的，即除了通过α-肾上腺素受体介导的神经刺激对去甲肾上腺素释放的突触前负反馈机制外，在肾上腺素能神经末梢中还存在通过激活突触前β-肾上腺素受体而触发的正反馈机制。
1 The effects of isoprenaline, propranolol and phentolamine, were studied on tritiated noradrenaline overflow elicited by postganglionic nerve stimulation in guinea-pig isolated atria. 2 Isoprenaline (1.2 times 10-minus 8M) increased while propranolol (1.0 times 10-minus 7M) reduced the overflow of tritiated noradrenaline evoked by nerve stimulation. These effects were less than those of phentolamine (3.1 times 10-minus 6M), which increased by approximately three-fold the overflow of [3H]-noradrenaline elicited by nerve stimulation. 3 Neuronal accumulation of tritiated noradrenaline in guinea-pig atria was not affected by isoprenaline, propranolol or phentolamine at the concentration employed in this study. 4 Isoprenaline (1.2 times 10-minus 8M) induced a positive chronotropic effect of about 80 percent of the maximum. On the other hand, propranolol produced a shift to the right in the frequency-response curve to nerve stimulation and in the concentration-response curve to exogenous noradrenaline in guinea-pig atria. 5 In the isolated nictitating membrane of the cat, the frequency-response curve to nerve stimulation was not modified by propranolol, while in the presence of 3.9 times 10-minus 6M of N,-2-(2,6-dimethylphenoxy)propyl-N,N,N-trimethylammonium (beta-methyl-TM 10) there was a shift to the right and a depression of slope. Neither propranolol nor beta-methyl-TM 10 affected responses to exogenous noradrenaline. 6. The effects of isoprenaline and of propranolol on transmitter release are compatible with the view that in addition to the presynaptic negative feed-back mechanism for noradrenaline release by nerve stimulation mediated via alpha-adrenoceptors a positive feed-back mechanism exists in adrenergic nerve endings which is triggered through the activation of presynaptic beta-adrenoceptors.