Jiménez R R, López M G, Sancho C, Maroto R, García A G
Departamento de Farmacología, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.
Biochem Biophys Res Commun. 1993 Mar 31;191(3):1278-83. doi: 10.1006/bbrc.1993.1355.
Acetylcholine (ACh, 100 microM)-evoked catecholamine release from perfused bovine adrenal glands was unaffected by CTX (0.3 microM) and depressed 70% by nisoldipine (1 microM). Combined CTX plus nisoldipine did not inhibit further the secretory response K+ (150 mM)-evoked secretion was diminished 30% by CTX and 20% by nisoldipine. Combined CTX plus nisoldipine inhibited secretion by 35%. Cd2+ blocked the K(+)-evoked secretory response by over 90%. Bay K 8644 (1 microM) enhanced the basal output of catecholamines and clearly potentiated the secretory responses to mild concentrations of ACh (3 microM) or K+ (17.7 mM). The results suggest that in addition to CTX- and DHP-sensitive Ca2+ channels, a third Ca2+ pathway might contribute to the entry of external Ca2+ into chromaffin cells necessary to trigger the exocytotic catecholamine release response in the bovine adrenal gland.
乙酰胆碱（ACh，100微摩尔）诱发的灌注牛肾上腺儿茶酚胺释放不受CTX（0.3微摩尔）影响，但被尼索地平（1微摩尔）抑制70%。CTX加尼索地平联合用药并未进一步抑制分泌反应，K+（150毫摩尔）诱发的分泌被CTX抑制30%，被尼索地平抑制20%。CTX加尼索地平联合用药抑制分泌35%。Cd2+阻断K+诱发的分泌反应超过90%。Bay K 8644（1微摩尔）增强了儿茶酚胺的基础分泌量，并明显增强了对低浓度ACh（3微摩尔）或K+（17.7毫摩尔）的分泌反应。结果表明，除了对CTX和二氢吡啶敏感的Ca2+通道外，第三条Ca2+途径可能有助于细胞外Ca2+进入嗜铬细胞，这对于触发牛肾上腺中儿茶酚胺释放的胞吐反应是必需的。
