Knepel W, Schöfl C
Department of Pharmacology, University of Freiburg im Breisgau, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1987 Sep;336(3):321-6. doi: 10.1007/BF00172685.
Arginine-vasopressin (AVP) stimulates adrenocorticotropin and beta-endorphin release from corticotrophs of the anterior pituitary gland through mechanisms which are not initiated by an elevation of the cellular levels of adenosine-3',5'-cyclic-monophosphate. In the present study the effect of AVP on the cytoplasmic concentrations of free calcium ions in rat anterior pituitary cells was examined. Cytosolic free Ca2+ concentrations were monitored directly using the new, intracellularly trapped fluorescent indicator fura-2. In cells incubated in medium containing 1.3 mmol/l Ca2+, AVP (100 nmol/l) caused an immediate elevation of the cytoplasmic Ca2+ concentration by about 50 nmol/l (P less than 0.001). The intracellular Ca2+ levels remained elevated during the observation period of 2-3 min. This effect of AVP was blocked by a specific vasopressin antagonist. By contrast, the glucocorticoid dexamethasone did not affect the AVP-induced elevation of cytosolic Ca2+ concentration. When the cells were incubated in Ca2+-free medium (Ca2+ omitted, EGTA 2 mmol/l), the AVP-induced as well as the K+ depolarization-induced increase in free cytoplasmic Ca2+ were abolished, whereas the ionophore ionomycin evoked a rapid transient elevation of free Ca2+. The increase in cytoplasmic Ca2+ concentration induced by AVP was preserved in medium containing the calcium channel blockers Mg2+ (Mg2+ 31.2 mmol/l; Ca2+ 1.3 mmol/l) or nifedipine (1 mumol/l). The potassium-evoked calcium signal was blocked by Mg2+ (31.2 mmol/l). We conclude that vasopressin induces a rapid rise in the cytoplasmic concentration of free calcium ions in corticotrophs. Vasopressin may mobilize calcium through mechanisms that neither are glucocorticoid-sensitive nor involve the influx of extracellular calcium through voltage-dependent calcium channels.(ABSTRACT TRUNCATED AT 250 WORDS)
精氨酸加压素（AVP）通过并非由细胞内3',5'-环磷酸腺苷水平升高引发的机制，刺激垂体前叶促肾上腺皮质激素细胞释放促肾上腺皮质激素和β-内啡肽。在本研究中，检测了AVP对大鼠垂体前叶细胞胞质中游离钙离子浓度的影响。使用新型的细胞内捕获荧光指示剂fura-2直接监测胞质游离Ca2+浓度。在含有1.3 mmol/L Ca2+的培养基中孵育的细胞，AVP（100 nmol/L）可使胞质Ca2+浓度立即升高约50 nmol/L（P<0.001）。在2 - 3分钟的观察期内，细胞内Ca2+水平持续升高。AVP的这种作用被特异性加压素拮抗剂阻断。相比之下，糖皮质激素地塞米松不影响AVP诱导的胞质Ca2+浓度升高。当细胞在无Ca2+培养基（省略Ca2+，2 mmol/L EGTA）中孵育时，AVP诱导的以及K+去极化诱导的胞质游离Ca2+增加均被消除，而离子载体离子霉素可引起游离Ca2+的快速短暂升高。在含有钙通道阻滞剂Mg2+（31.2 mmol/L；Ca2+ 1.3 mmol/L）或硝苯地平（1 μmol/L）的培养基中，AVP诱导的胞质Ca2+浓度升高得以保留。Mg2+（31.2 mmol/L）可阻断钾诱导的钙信号。我们得出结论，加压素可诱导促肾上腺皮质激素细胞胞质中游离钙离子浓度迅速升高。加压素可能通过既不依赖糖皮质激素也不涉及细胞外钙通过电压依赖性钙通道内流的机制来动员钙。（摘要截短于250字）
