Bird I M, Lightly E R, Nicol M, Williams B C, Walker S W
Dept. Ob/Gyn, Univ. WI-Madison, 53715, USA.
Endocr Res. 1998 Aug-Nov;24(3-4):769-72. doi: 10.3109/07435809809032685.
Previous reports have suggested a possible dopaminergic inhibition of the actions of AII on aldosterone secretion via adenylate-cyclase inhibitory 'D2' receptors. Others suggest a possible stimulation of aldosterone secretion via a stimulatory 'D1' receptor/cAMP pathway. We have examined the actions of dopamine on basal and AII-stimulated cortisol secretion by cultured bovine zfr cells. Dopamine alone caused a dose-dependent increase in cortisol secretion at doses >10(-5) M, and also enhanced steroidogenic output in response to submaximal (10(-10) M) but not maximal (10(-8) M) stimulatory doses of AII. The stimulatory action of dopamine alone on cortisol secretion was not, however, reproduced by the 'D1' agonist fenoldopam, and was fully blocked by propranolol. Dopamine had neither a stimulatory effect on basal phosphoinositol production nor an inhibitory effect on AII-stimulated phosphoinositol production. Our findings are therefore inconsistent with the activation of a 'D1' or 'D2' class receptor, and suggest the stimulation of cortisol secretion occurred nonspecifically through a beta-adrenergic receptor.
先前的报道表明，多巴胺可能通过抑制腺苷酸环化酶的“D2”受体，对血管紧张素II（AII）作用于醛固酮分泌产生抑制。其他研究则提示，多巴胺可能通过刺激性的“D1”受体/cAMP途径刺激醛固酮分泌。我们研究了多巴胺对培养的牛zfr细胞基础状态及AII刺激的皮质醇分泌的作用。单独使用多巴胺时，剂量>10(-5)M时可引起皮质醇分泌呈剂量依赖性增加，并且在亚最大刺激剂量（10(-10)M）而非最大刺激剂量（10(-8)M）的AII作用下，可增强类固醇生成输出。然而，“D1”激动剂非诺多泮并不能重现多巴胺单独对皮质醇分泌的刺激作用，且该作用被普萘洛尔完全阻断。多巴胺对基础磷酸肌醇生成既无刺激作用，对AII刺激的磷酸肌醇生成也无抑制作用。因此，我们的研究结果与“D1”或“D2”类受体的激活不一致，提示皮质醇分泌的刺激是通过β-肾上腺素能受体非特异性发生的。
