Schrey M P, Read A M
Department of Chemical Pathology, St Mary's Hospital Medical School, University of London, U.K.
Mol Cell Endocrinol. 1988 May;57(1-2):107-13. doi: 10.1016/0303-7207(88)90039-1.
The production of inositol phosphates in response to carbachol was studied in rat anterior pituitary tissue prelabelled with [3H]inositol. Carbachol (10 microM) stimulated inositol mono-, bis- and trisphosphate production (IP1, IP2 and IP3) by 360 +/- 49, 338 +/- 49 and 503 +/- 49 (mean +/- SEM, P less than 0.001) percent respectively during a 30 min incubation. Mean basal production was 5.4 +/- 0.3, 4.1 +/- 0.5 and 0.9 +/- 0.3 expressed as a percent of total [3H]inositol lipid for IP, IP2 and IP3 respectively. Stimulated inositol phosphate production was dose dependent and detectable after 5 min. Atropine prevented this stimulation indicating mediation via muscarinic receptors. Removal of extracellular Ca2+ reduced both basal and stimulated total inositol phosphate production by 60% and 56% respectively but did not impair carbachol-induced phosphoinositide hydrolysis per se. Pretreatment of pituitary tissue with either somatostatin (5 micrograms/ml) or pertussis toxin (1 microgram/ml) had no effect on either basal or stimulated inositol phosphate production. These results demonstrate a cholinergic stimulation of phosphatidylinositol bisphosphate (PIP2) hydrolysis in the anterior pituitary which may be important in the action of cholinergic agonists on pituitary hormone secretion.
在预先用[3H]肌醇标记的大鼠垂体前叶组织中,研究了对卡巴胆碱产生的肌醇磷酸的生成情况。在30分钟的孵育过程中,卡巴胆碱(10微摩尔)分别刺激肌醇一磷酸、二磷酸和三磷酸(IP1、IP2和IP3)的生成,刺激幅度分别为360±49%、338±49%和503±49%(平均值±标准误,P<0.001)。以占总[3H]肌醇脂质的百分比表示,IP1、IP2和IP3的平均基础生成量分别为5.4±0.3%、4.1±0.5%和0.9±0.3%。刺激后的肌醇磷酸生成呈剂量依赖性,5分钟后即可检测到。阿托品可阻止这种刺激,表明是通过毒蕈碱受体介导的。去除细胞外Ca2+分别使基础和刺激后的总肌醇磷酸生成量降低60%和56%,但并不损害卡巴胆碱诱导的磷酸肌醇水解本身。用生长抑素(5微克/毫升)或百日咳毒素(1微克/毫升)预处理垂体组织,对基础或刺激后的肌醇磷酸生成均无影响。这些结果表明,垂体前叶中磷脂酰肌醇二磷酸(PIP2)水解受到胆碱能刺激,这可能在胆碱能激动剂对垂体激素分泌的作用中起重要作用。