Marks R, Barlow J W, Funder J W
J Clin Endocrinol Metab. 1982 May;54(5):1075-7. doi: 10.1210/jcem-54-5-1075.
Two currently used steroids (clobetasone butyrate and betamethasone valerate) reproducibly cause vasoconstriction on topical application to human forearm skin. Progesterone, deoxycorticosterone, testosterone, and estradiol, even at 100- to 200-fold higher concentrations, cause no vasoconstriction when applied alone. Applied with clobestasone butyrate, testosterone and estradiol are without antagonist effect; in contrast, both progesterone and deoxycorticosterone antagonize the vasoconstrictor response in a dose-related fashion, with a half-maximal effect at 20-30 times the concentration of clobetasone. Neither progesterone nor deoxycorticosterone affects the vasoconstriction produced by the intradermal injection of epinephrine. In most glucocorticoid-responsive systems, progesterone and deoxycorticosterone are glucocorticoid antagonists, and estradiol and testosterone are inactive. We interpret these studies as evidence that the vasoconstrictor effects of topical steroids are mediated by occupancy of classical glucocorticoid receptors, rather than by nonspecific pharmacological mechanisms.
目前使用的两种类固醇（丁酸氯倍他松和戊酸倍他米松）局部应用于人体前臂皮肤时可重复性地引起血管收缩。孕酮、脱氧皮质酮、睾酮和雌二醇，即使浓度高出100至200倍，单独应用时也不会引起血管收缩。与丁酸氯倍他松联合应用时，睾酮和雌二醇无拮抗作用；相反，孕酮和脱氧皮质酮均以剂量相关的方式拮抗血管收缩反应，在浓度为丁酸氯倍他松20至30倍时产生半数最大效应。孕酮和脱氧皮质酮均不影响皮内注射肾上腺素所产生的血管收缩。在大多数糖皮质激素反应系统中，孕酮和脱氧皮质酮是糖皮质激素拮抗剂，而雌二醇和睾酮无活性。我们将这些研究解释为局部类固醇的血管收缩作用是由经典糖皮质激素受体的占据介导的，而非非特异性药理机制的证据。
