Coronary Artery Spasm, Hypertension, Hypokalemia and Licorice
Coronary Artery Spasm, Hypertension, Hypokalemia and Licorice
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DOI：
10.4172/2165-7920.1000143
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发表时间：
2012-05
期刊：
影响因子：
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通讯作者：
E. Konik;Emily G. Kurtz;F. Sam;D. Sawyer
中科院分区：
文献类型：
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作者：
E. Konik;Emily G. Kurtz;F. Sam;D. Sawyer
高血压伴低钾血症，特别是在停用利尿剂的患者中，提示由于盐皮质激素活性增加而引起的继发性高血压，例如，原发性肾素、醛固酮或非醛固酮盐皮质激素分泌增加或盐皮质激素样作用增加。盐皮质激素受体（MR）优先结合皮质醇。皮质醇的盐皮质激素效应在某些组织中通过表达11-β羟类固醇脱氢酶2（11 BHSD 2）来避免，该酶负责将皮质醇转化为其11-酮衍生物（可的松），其对MR受体具有最小亲和力。只有当皮质醇转化为无活性的可的松时，醛固酮才能与MR结合。罕见的先天性11 BHSD 2缺乏症或甘草消耗对其的抑制模拟了醛固酮增多症状态。
Hypertension with hypokalemia, especially in a patient off diuretics, suggests a secondary hypertension due to an increase in mineralocorticoid activity, for example, primary increases in renin, aldosterone, or nonaldosterone mineralocorticoid secretion or an increased mineralocorticoid-like effect. Mineralocorticoid Receptors (MR) preferentially bind cortisol. A mineralocorticoid effect of cortisol is avoided in some tissues by expression of 11-Beta Hydroxysteroid Dehydrogenase type 2 (11 BHSD2), the enzyme responsible for transformation of cortisol to its 11-keto derivative (cortisone), which has minimal affinity for MR receptors. Only when cortisol is converted to the inactive cortisone can aldosterone bind to the MR. Rare congenital deficiency of 11 BHSD2 or its inhibition by licorice consumption mimics hyperaldosteronic state.