Elliott M E, Goodfriend T L
Fed Proc. 1986 Aug;45(9):2376-81.
Atrial natriuretic factor (ANF) inhibits basal and stimulated aldosterone synthesis in adrenal glomerulosa cells. ANF probably acts through specific membrane receptors. Alterations in cyclic GMP and cyclic AMP levels do not account for ANF's inhibitory effect. ANF does not block angiotensin II (AngII) receptors nor does it interfere with phosphoinositide metabolism or calcium movements stimulated by adrenal agonists. ANF does not inhibit protein synthesis nor does it work by inhibiting NA+,K+-ATPase or depleting cell potassium. ANF decreases conversion of endogenous cholesterol to pregnenolone, the step stimulated by adrenocorticotropin and AngII. ANF does not affect the conversion of 20-alpha-hydroxycholesterol, which easily penetrates mitochondrial membranes to the site of the cholesterol side-chain cleavage enzyme. These results suggest that ANF inhibits the ability of endogenous cholesterol to reach or interact with the side-chain cleavage enzyme. ANF does not act like a calcium channel-blocking agent. However, ANF is less effective at high-calcium concentrations, which suggests that it may inhibit a step that calcium stimulates. Understanding ANF action will probably require identification of the specific biochemical changes (mediators) that it induces. Parallel efforts to understand how other agents stimulate steroidogenesis (particularly in the areas of protein synthesis, protein phosphorylation, and cholesterol movements) will further this understanding.
心房利钠因子（ANF）可抑制肾上腺球状带细胞基础状态及受刺激状态下的醛固酮合成。ANF可能通过特异性膜受体发挥作用。环磷酸鸟苷（cGMP）和环磷酸腺苷（cAMP）水平的改变并不能解释ANF的抑制作用。ANF既不阻断血管紧张素II（AngII）受体，也不干扰肾上腺激动剂刺激的磷酸肌醇代谢或钙转运。ANF既不抑制蛋白质合成，也不是通过抑制钠钾ATP酶或消耗细胞内钾发挥作用。ANF可减少内源性胆固醇向孕烯醇酮的转化，而这一步骤是由促肾上腺皮质激素和AngII刺激的。ANF不影响20-α-羟基胆固醇的转化，20-α-羟基胆固醇可轻易穿透线粒体膜到达胆固醇侧链裂解酶的作用位点。这些结果表明，ANF抑制内源性胆固醇到达或与侧链裂解酶相互作用的能力。ANF的作用方式不像钙通道阻滞剂。然而，在高钙浓度下ANF的作用效果较差，这表明它可能抑制了钙所刺激的某个步骤。要了解ANF的作用可能需要鉴定其诱导的特定生化变化（介质）。同时致力于了解其他因子如何刺激类固醇生成（特别是在蛋白质合成、蛋白质磷酸化和胆固醇转运方面）将有助于这一理解。
