減塩時の, ACTHに対するアルド久テロン反応性におよぼす内因性プロスタグランジンの影響

スポンサーリンク

概要

• 論文の詳細を見る

• Aldosterone production following ACTH administration has been shown to be enhanced in sodium depletion. The mechanism (s) for this, however, is not entirely clear. Meanwhile, prostaglandins of the E series have been shown to stimulate steroidogenesis and urinary excretion of prostaglandin E<SUB>2</SUB> and F<SUB>2α</SUB> in man, and PGI<SUB>2</SUB> in the aortic wall of rats has been shown to increase in sodium depletion.<BR>In view of the above findings the present study was undertaken to evaluate the involvement of the endogenous prostaglandins in the augmentation of ACTH-induced aldosterone response during acute sodium depletion. Captopril was administered to elucidate the influence of the renin-angiotensin system (250mg q.i.d.) and Indomethacin (Ind) to suppress the production of the endogenous prostaglandins (200mg q.i.d.). Group I were on a diet containing 200mEq/day sodium and sodium depletion was achieved by a low sodium diet containing 60mEq/day sodium and oral treatment of fulosemide 80mg for 1 day (groups II, III and IV). Ind was given in group II, Ind + captopril in group III and captopril in group IV. The i.m. administration of 250μg ACTH was performed at 0800-0900h.<BR>Body weight, serum sodium and potassium levels on the day of the experiment were significantly lower in groups II, III and IV versus group I. Basal PRA. in groups III and IV were more significantly elevated than groups I and II. Basal plasma 6-keto-PGF<SUB>1α</SUB> levels were significantly lower than in the Ind pretreated groups (II, III). There were no significant differences between baseline plasma aldosterone and cortisol concentrations.<BR>In groups I, II and III, plasma aldosterone increased from baseline levels to 182%, 134%, 193% respectively, following the ACTH administration, and there were no significant differences in mean increment among the three groups. In group IV, however, plasma aldosterone increased from 6.4 ± 0.9 ng/dl to 32.1 ± 4.9ng/dl and 26.1 ± 3.9 ng/dl at 30 and 60 min. after the ACTH administration respectively, a mean increment of 468%. This response was significantly greater than those of the three other groups. Plasma cortisol response to ACTH administration was similar in all four groups. The augmented response to ACTH was not affected by angiotensin I converting enzyme inhibitor, captopril however, significantly reduced the response in Ind pretreated groups.<BR>It is suggested that endogenous prostaglandins may modulate augmented ACTH induced aldosterone response in a sodium depleted state in man.

• 日本内分泌学会の論文

著者

• 森瀬 敏夫

  金沢大学医学部内科学第二講座

関連論文

• 0920 シクロスポリン高血圧に対するNeutral endopeptidase阻害薬長期投与による降圧効果
• 続発性ヘモクロマトーシスの進展とともに下垂体gonadotrohと膵β細胞に選択的障害をきたした1例
• うっ血性心不全患者におけるナトリウム利尿因子
• 63) 冠攣縮性狭心症におけるACE遺伝子多型性
• P439 カルシウム拮抗薬およびACE阻害薬の自律神経系に及ぼす影響 : 心拍・血圧変動のスペクトラム解析による検討
• Klinefelter症候群に発症した多ホルモン産生性 (GH, TSH, PRL) 下垂体腺腫の1例
• 副腎皮質女性化腫瘍の1例
• 巨大血小板性血小板減少症・難聴・腎炎および白内障を合併した遺伝性疾患の1家系
• 無麻酔家兎におけるプロスタサイクリン (PGI2) の血圧調節およびアルドステロン分泌に果たす役割り
• 減塩時の, ACTHに対するアルド久テロン反応性におよぼす内因性プロスタグランジンの影響
• 6-oxo-prostaglandin E1のヒトにおけるレニン・アンジオテンシン・アルドステロン系, 血圧, 血小板凝集能に及ぼす影響
• 本態性高血圧症および各種二次性高血圧症における循環血液量

もっと見る 閉じる

スポンサーリンク