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糖皮质激素与血压:皮质醇/可的松穿梭机制在人体血管张力控制中的作用

Glucocorticoids and blood pressure: a role for the cortisol/cortisone shuttle in the control of vascular tone in man.

作者信息

Walker B R, Connacher A A, Webb D J, Edwards C R

机构信息

University of Edinburgh, Department of Medicine, Western General Hospital, Scotland, U.K.

出版信息

Clin Sci (Lond). 1992 Aug;83(2):171-8. doi: 10.1042/cs0830171.

Abstract
  1. 11 beta-Hydroxysteroid dehydrogenase converts cortisol to inactive cortisone in man. In distal renal tubules, this inactivation protects mineralocorticoid receptors from cortisol. Congenital 11 beta-hydroxysteroid dehydrogenase deficiency and inhibition of 11 beta-hydroxysteroid dehydrogenase by liquorice or carbenoxolone result in cortisol-dependent hypokalaemia and hypertension. 2. 11 beta-Hydroxysteroid dehydrogenase is expressed in vascular smooth muscle. Both glucocorticoids and mineralocorticoids potentiate vascular responses to noradrenaline. 11 beta-Hydroxysteroid dehydrogenase activity may therefore influence vascular tone. 3. Experiments were performed in healthy subjects with and without 7 days of oral administration of 11 beta-hydroxysteroid dehydrogenase inhibitors (liquorice or carbenoxolone), and in a patient with congenital 11 beta-hydroxysteroid dehydrogenase deficiency. We measured the following parameters: dermal vasoconstriction after topical application of cortisol, forearm blood flow during brachial artery infusion of cortisol or noradrenaline, and blood pressure during systemic infusion of noradrenaline. 4. Cortisol-induced dermal vasoconstriction was increased by liquorice (23 +/- 6 to 52 +/- 7 units; P < 0.04) and in congenital 11 beta-hydroxysteroid dehydrogenase deficiency (87 units). In congenital 11 beta-hydroxysteroid dehydrogenase deficiency intraarterial infusion of cortisol caused vasoconstriction (20% reduction in blood flow in the infused arm) and accentuated the response to application of lower-body negative pressure, which stimulates sympathetically mediated vasoconstriction (35% reduction). However, intra-arterial infusion of cortisol had no effect in healthy subjects either with or without administration of liquorice. 5. Carbenoxolone potentiated both noradrenaline induced forearm vasoconstriction (P < 0.01) and pressor response (P < 0.001). 6. We conclude that 11 beta-hydroxysteroid dehydrogenase modulates the access of cortisol to vascular receptors and thereby influences vascular sensitivity to noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 11β-羟类固醇脱氢酶可将人体内的皮质醇转化为无活性的可的松。在远端肾小管中,这种失活作用可保护盐皮质激素受体免受皮质醇影响。先天性11β-羟类固醇脱氢酶缺乏以及甘草或甘珀酸对11β-羟类固醇脱氢酶的抑制作用会导致皮质醇依赖性低钾血症和高血压。2. 11β-羟类固醇脱氢酶在血管平滑肌中表达。糖皮质激素和盐皮质激素均可增强血管对去甲肾上腺素的反应。因此,11β-羟类固醇脱氢酶活性可能会影响血管张力。3. 对健康受试者进行了实验,部分受试者口服11β-羟类固醇脱氢酶抑制剂(甘草或甘珀酸)7天,部分未服用,同时也对一名先天性11β-羟类固醇脱氢酶缺乏的患者进行了实验。我们测量了以下参数:局部应用皮质醇后的皮肤血管收缩、肱动脉输注皮质醇或去甲肾上腺素期间的前臂血流量以及全身输注去甲肾上腺素期间的血压。4. 甘草(从23±6单位增至52±7单位;P<0.04)以及先天性11β-羟类固醇脱氢酶缺乏(87单位)均使皮质醇诱导的皮肤血管收缩增强。在先天性11β-羟类固醇脱氢酶缺乏患者中,动脉内输注皮质醇会引起血管收缩(输注侧手臂血流量减少20%),并增强对下体负压应用的反应,下体负压可刺激交感神经介导的血管收缩(血流量减少35%)。然而,无论是否服用甘草,动脉内输注皮质醇对健康受试者均无影响。5. 甘珀酸增强了去甲肾上腺素诱导的前臂血管收缩(P<0.01)和升压反应(P<0.001)。6. 我们得出结论,11β-羟类固醇脱氢酶可调节皮质醇与血管受体的结合,从而影响血管对去甲肾上腺素的敏感性。(摘要截短至250字)

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