Grau E G, Nishioka R S, Bern H A
Endocrinology. 1982 Mar;110(3):910-5. doi: 10.1210/endo-110-3-910.
Both somatostatin (SRIF) and urotensin II, a dodecapeptide from the teleost caudal neurosecretory system, inhibit PRL release from the organ-cultured rostral pars distalis of the tilapia, Sarotherodon mossambicus, in a dose-related manner. The inhibitory action of SRIF on PRL release was completely prevented by the presence of the calcium ionophore A23187. PRL release was also blocked when Ca++ was excluded from the incubation medium, even in the presence of the ionophore. Both dibutyryl cAMP (dbcAMP) and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, alone or in combination, stimulated PRL release during incubation in high osmotic pressure medium. The effect of dbcAMP appeared to be dose related. Together, dbcAMP and 3-isobutyl-1-methylxanthine were also effective in preventing the inhibition of PRL release by SRIF. These results are consistent with the notion that Ca++, and possibly cAMP, may be important mediators of PRL secretion, and it is likely that SRIF may inhibit PRL release by blocking a Ca++- or cAMP-mediated mechanism.
生长抑素(SRIF)和硬骨鱼尾部神经分泌系统的一种十二肽——尾加压素II,均以剂量相关的方式抑制来自莫桑比克罗非鱼(Sarotherodon mossambicus)器官培养的吻端远侧部的催乳素释放。钙离子载体A23187的存在完全阻止了SRIF对催乳素释放的抑制作用。即使存在离子载体,当孵育培养基中不含Ca++时,催乳素释放也会被阻断。在高渗培养基孵育期间,二丁酰环磷腺苷(dbcAMP)和磷酸二酯酶抑制剂3 - 异丁基 - 1 - 甲基黄嘌呤单独或联合使用均刺激催乳素释放。dbcAMP的作用似乎与剂量相关。此外,dbcAMP和3 - 异丁基 - 1 - 甲基黄嘌呤在防止SRIF对催乳素释放的抑制方面也有效。这些结果与以下观点一致,即Ca++以及可能的cAMP可能是催乳素分泌的重要介质,并且SRIF可能通过阻断Ca++或cAMP介导的机制来抑制催乳素释放。