EFFECT OF ATRIAL PEPTIDES ON ALDOSTERONE PRODUCTION
EFFECT OF ATRIAL PEPTIDES ON ALDOSTERONE PRODUCTION
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DOI：
10.1172/jci112172
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发表时间：
1985-01-01
影响因子：
15.9
通讯作者：
FRANCOSAENZ, R
中科院分区：
文献类型：
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作者：
ATARASHI, K;MULROW, PJ;FRANCOSAENZ, R
本研究用大鼠肾上腺细胞悬液研究了合成心房肽（心房肽Ⅰ、Ⅱ和Ⅲ）对醛固酮和皮质酮产生的影响。此外，我们研究了心房肽II输注对大鼠血浆醛固酮对血管紧张素II反应的影响。心房肽I、II和III以剂量依赖性方式降低肾小球上皮细胞的醛固酮释放。10 pM的心房肽II显著抑制基础醛固酮释放（P < 0.01），10 nM的心房肽II或III使其降低79%。心房肽II降低肾小球细胞对促肾上腺皮质激素（ACTH）和血管紧张素II的敏感性。心房肽II对基础或ACTH刺激的束状体-髓质细胞皮质酮释放没有影响。在体内输注血管紧张素II与或不同时输注心房肽素II显示，心房肽素II显着抑制醛固酮反应血管紧张素II。心房肽II的这种抑制作用不依赖于对血浆肾素活性、血清钾或ACTH的任何影响。这些数据提高了心房利钠肽可能影响肾脏的钠排泄的可能性，不仅直接，而且通过抑制醛固酮的产生间接。
This sutdy examines the effects of the synthetic atrial peptides (atriopeptin I, II, and III) on aldosterone and corticosterone production by rat adrenal cell suspensions. Furthermore, we studied the effect of atriopeptin II infusion on the plasma aldosterone response to angiotensin II in the rat in vivo. Atriopeptin I, II, and III decreased aldosterone release from zona glomerulosa cells in a dose-dependent fashion. 10 pM atriopeptin II inhibited basal aldosterone release significantly (P < 0.01), and 10 nM atriopeptin II or III lowered it by 79%. Atriopeptin II decreased the sensitivity of the glomerulosa cells to adrenocorticotropic hormone (ACTH) and angiotensin II. Atriopeptin II had no effect on basal or ACTH-stimulated corticosterone release by fasciculata-medullary cells. In vivo infusions of angiotensin II with or without simultaneous infusions of atriopeptin II showed that atriopeptin II significantly inhibited the aldosterone response to angiotensin II. This inhibition by atriopeptin II was independent of any effect on plasma renin activity, serum potassium, or ACTH. These data raise the possibility that the atrial natriuretic peptides may affect sodium excretion by the kidney, not only directly, but also indirectly through the inhibition of aldosterone production.