Watlington C O, Kramer L B, Schuetz E G, Zilai J, Grogan W M, Guzelian P, Gizek F, Schoolwerth A C
Division of Endocrinology and Metabolism, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0145.
Am J Physiol. 1992 Jun;262(6 Pt 2):F927-31. doi: 10.1152/ajprenal.1992.262.6.F927.
Evidence for increased glucocorticoid 6 beta-hydroxylation (enhanced family 3A cytochrome P-450 activity) is found in certain reversible forms of human hypertension. This association was investigated in the spontaneously hypertensive rat (SHR). The proportion of injected [3H]corticosterone excreted in urine as 6 beta-[3H]OH-corticosterone was four- to fivefold higher in SHR than in control Wistar-Kyoto rats, before and after development of overt hypertension. Both hypertension and 6 beta-hydroxylation were inhibited by troleandomycin (a selective inhibitor of family 3A cytochromes P-450), consistent with a role for increased steroid 6 beta-hydroxylation in the genesis of hypertension in the SHR.
在某些可逆性人类高血压类型中发现了糖皮质激素6β-羟化增加（细胞色素P-450 3A家族活性增强）的证据。在自发性高血压大鼠（SHR）中对这种关联进行了研究。在明显高血压形成之前和之后，SHR尿中作为6β-[³H]羟基皮质酮排泄的注射[³H]皮质酮比例比对照Wistar-Kyoto大鼠高4至5倍。曲古抑菌素（细胞色素P-450 3A家族的选择性抑制剂）可抑制高血压和6β-羟化，这与类固醇6β-羟化增加在SHR高血压发生中的作用一致。
