Narayanan N, Lussier B, French M, Moor B, Kraicer J
Department of Physiology, University of Western Ontario, London, Canada.
Endocrinology. 1989 Jan;124(1):484-95. doi: 10.1210/endo-124-1-484.
The purpose of this study was to characterize the adenylate cyclase system in a purified population of normal somatotrophs derived from rat pituitary and to determine the responses of this system to GRF, somatostatin, guanine nucleotides, and cations. Additionally, experiments were performed to evaluate the interrelationships among changes in adenylate cyclase activity, cellular cAMP levels, and GH release induced by GRF and somatostatin. The results obtained using homogenates and membrane preparations from somatotrophs included the following. 1) GRF caused guanine nucleotide-dependent concentration-related (Ka, approximately 10(-8) M) stimulation of adenylate cyclase activity. 2) Guanine nucleotides were effective in stimulating cyclase in the absence of GRF; the concentration of guanine nucleotide required for half-maximal stimulation was decreased more than 10-fold in the presence of GRF. 3) Adenylate cyclase activity increased with increasing concentrations of free Mg2+ (0.25-20 mM); activation by GRF and guanine nucleotide resulted in an approximately 7-fold increase in the enzyme's affinity for free Mg2+. 4) Somatostatin, up to 10(-6) M, did not alter basal or GRF-stimulated adenylate cyclase activity. 5) Ca2+ (0.5-11.9 microM) produced concentration-dependent inhibition of basal (up to 28%) and GRF-stimulated (up to 47%) cyclase activities; the inhibitory effect of Ca2+ was accompanied by a decrement (2- to 3-fold) in the apparent affinities of the enzyme for both GRF and guanine nucleotide. In intact somatotrophs, GRF produced concentration-dependent stimulation of GH release (Ka, approximately 6 x 10(-11) M), preceded by a marked elevation of cAMP levels. While somatostatin blocked GRF-induced GH release, the augmented cAMP levels were only slightly reduced.(ABSTRACT TRUNCATED AT 400 WORDS)
本研究的目的是对源自大鼠垂体的纯化正常生长激素分泌细胞群体中的腺苷酸环化酶系统进行特性分析,并确定该系统对生长激素释放因子(GRF)、生长抑素、鸟嘌呤核苷酸和阳离子的反应。此外,还进行了实验以评估GRF和生长抑素诱导的腺苷酸环化酶活性变化、细胞内cAMP水平变化与生长激素(GH)释放之间的相互关系。使用生长激素分泌细胞的匀浆和膜制剂获得的结果如下:1)GRF引起鸟嘌呤核苷酸依赖性的浓度相关(Ka,约10^(-8) M)的腺苷酸环化酶活性刺激。2)在没有GRF的情况下,鸟嘌呤核苷酸能有效刺激环化酶;在存在GRF的情况下,半最大刺激所需的鸟嘌呤核苷酸浓度降低了10倍以上。3)腺苷酸环化酶活性随游离Mg2+浓度(0.25 - 20 mM)的增加而增加;GRF和鸟嘌呤核苷酸的激活导致该酶对游离Mg2+的亲和力增加约7倍。4)高达10^(-6) M的生长抑素不会改变基础或GRF刺激的腺苷酸环化酶活性。5)Ca2+(0.5 - 11.9 microM)产生浓度依赖性的基础(高达28%)和GRF刺激(高达47%)环化酶活性抑制;Ca2+的抑制作用伴随着该酶对GRF和鸟嘌呤核苷酸的表观亲和力下降(2至3倍)。在完整的生长激素分泌细胞中,GRF产生浓度依赖性的GH释放刺激(Ka,约6×10^(-11) M),之前cAMP水平显著升高。虽然生长抑素阻断GRF诱导的GH释放,但升高的cAMP水平仅略有降低。(摘要截断于400字)