Atarashi K, Mulrow P J, Franco-Saenz R
J Clin Invest. 1985 Nov;76(5):1807-11. doi: 10.1172/JCI112172.
This study 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 less than 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.
本研究检测了合成心房肽(心房肽素I、II和III)对大鼠肾上腺细胞悬液中醛固酮和皮质酮生成的影响。此外,我们还研究了在大鼠体内输注心房肽素II对血浆醛固酮对血管紧张素II反应的影响。心房肽素I、II和III以剂量依赖方式降低了球状带细胞中醛固酮的释放。10 pM心房肽素II显著抑制基础醛固酮释放(P小于0.01),10 nM心房肽素II或III使其降低79%。心房肽素II降低了球状带细胞对促肾上腺皮质激素(ACTH)和血管紧张素II的敏感性。心房肽素II对束状带-髓质细胞基础或ACTH刺激的皮质酮释放无影响。在体内输注血管紧张素II,无论是否同时输注心房肽素II,结果显示心房肽素II显著抑制醛固酮对血管紧张素II的反应。心房肽素II的这种抑制作用与对血浆肾素活性、血清钾或ACTH的任何影响无关。这些数据提示,心房利钠肽可能不仅直接影响肾脏排钠,还可能通过抑制醛固酮生成间接影响肾脏排钠。