Katoh F, Kitamura K, Niina H, Yamamoto R, Washimine H, Kangawa K, Yamamoto Y, Kobayashi H, Eto T, Wada A
Department of Internal Medicine, Miyazaki Medical College, Japan.
J Neurochem. 1995 Jan;64(1):459-61. doi: 10.1046/j.1471-4159.1995.64010459.x.
In cultured bovine adrenal medullary cells, stimulation of nicotinic receptors by carbachol evoked the Ca(2+)-dependent exocytotic cosecretion of proadrenomedullin N-terminal 20 peptide (PAMP) (EC50 = 50.1 microM) and catecholamines (EC50 = 63.0 microM), with the molar ratio of PAMP/catecholamines secreted being equal to the ratio in the cells. Addition of PAMP [1-20]NH2 inhibited carbachol-induced 22Na+ influx via nicotinic receptors (IC50 = 2.5 microM in a noncompetitive manner and thereby reduced carbachol-induced 45Ca2+ influx via voltage-dependent Ca2+ channels (IC50 = 1.0 microM) and catecholamine secretion (IC50 = 1.6 microM). It did not alter high K(+)-induced 45Ca2+ influx via voltage-dependent Ca2+ channels or veratridine-induced 22Na+ influx via voltage-dependent Na+ channels. PAMP seems to be a novel antinicotinic peptide cosecreted with catecholamines by a Ca(2+)-dependent exocytosis in response to nicotinic receptor stimulation.
在培养的牛肾上腺髓质细胞中，卡巴胆碱对烟碱样受体的刺激引发了肾上腺髓质素N端20肽（PAMP）（EC50 = 50.1微摩尔）和儿茶酚胺（EC50 = 63.0微摩尔）的钙依赖性胞吐共分泌，所分泌的PAMP/儿茶酚胺的摩尔比与细胞中的比例相等。添加PAMP [1-20]NH2以非竞争性方式抑制了卡巴胆碱诱导的通过烟碱样受体的22Na+内流（IC50 = 2.5微摩尔），从而减少了卡巴胆碱诱导的通过电压依赖性钙通道的45Ca2+内流（IC50 = 1.0微摩尔）和儿茶酚胺分泌（IC50 = 1.6微摩尔）。它并未改变高钾诱导的通过电压依赖性钙通道的45Ca2+内流或藜芦碱诱导的通过电压依赖性钠通道的22Na+内流。PAMP似乎是一种新型抗烟碱肽，在烟碱样受体刺激下通过钙依赖性胞吐作用与儿茶酚胺共分泌。
