Kudo M, Kudo T, Matsuki A
Department of Anesthesiology, University of Hirosaki School of Medicine.
Masui. 1991 Dec;40(12):1819-24.
In order to investigate the effects of prostaglandin E1 (PGE1) used in hypotensive anesthesia on the adrenal endocrine function, aldosterone, corticosterone (Comp B) and cAMP production were measured in isolated glomerulosa (G-c) and fasciculata cells (F-c) of the rats. Rat glomerulosa and fasciculata cells were obtained by enzymatic digestion of the adrenals of male wistar rats. The cell pellet was suspended in Hank's balanced salt solution containing 0.1% BSA and distributed in 900 microliters aliquots to polyethylene tubes. The samples were preincubated for 90 min in a 37 degrees C water bath aerated with 5% CO2/95% O2. PGE1 or ACTH 50 microliters was added and incubated for 4 hr. Total volume of the incubation medium is 1.0 ml. Aldosterone and cAMP were measured by radioimmunoassay and Comp B was determined by fluorimetric method. PGE1 increased significantly the basal secretion of aldosterone and Comp B in G-c and F-c, respectively. The steroidogenic effect of PGE1 was dose dependent in aldosterone production. This aldosterone production was also accompanied with cAMP production. On the other hand, significant increase of cAMP was not observed in comp B production. These results suggest that cAMP may be the second messenger in PGE1-induced aldosterone production in G-c. But PGE1 receptors in F-c seem not to be coupled to the adenylate cyclase system. The addition of ACTH and PGE1 resulted in inhibition of aldosterone secretion when compared with that obtained by ACTH alone. Several researchers have shown that low doses of PGE1 depressed the basal aldosterone secretion. These findings may be contributing to Na-uresis effect during PGE1-induced hypotension.
为了研究用于低血压麻醉的前列腺素E1(PGE1)对肾上腺内分泌功能的影响,我们检测了大鼠离体球状带(G-c)和束状带细胞(F-c)中醛固酮、皮质酮(化合物B)和环磷酸腺苷(cAMP)的生成情况。通过酶解雄性Wistar大鼠的肾上腺获取球状带和束状带细胞。将细胞沉淀悬浮于含0.1%牛血清白蛋白的汉克平衡盐溶液中,并分装成900微升的等分试样至聚乙烯管中。样本在37℃、含5%二氧化碳/95%氧气的水浴中预孵育90分钟。加入50微升PGE1或促肾上腺皮质激素(ACTH)并孵育4小时。孵育培养基总体积为1.0毫升。通过放射免疫分析法测定醛固酮和cAMP,用荧光法测定化合物B。PGE1分别显著增加了G-c和F-c中醛固酮和化合物B的基础分泌。PGE1的类固醇生成作用在醛固酮生成方面呈剂量依赖性。这种醛固酮生成也伴随着cAMP生成。另一方面,在化合物B生成中未观察到cAMP的显著增加。这些结果表明,cAMP可能是PGE1诱导G-c中醛固酮生成的第二信使。但F-c中的PGE1受体似乎未与腺苷酸环化酶系统偶联。与单独使用ACTH相比,同时加入ACTH和PGE1会导致醛固酮分泌受到抑制。几位研究人员已表明,低剂量的PGE1会抑制基础醛固酮分泌。这些发现可能有助于解释PGE1诱导低血压期间的利钠作用。