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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Ingram M C, Wallace A M, Collier A, Fraser R, Connell J M

MRC Blood Pressure Unit, Western Infirmary, Glasgow, Scotland.

Clin Exp Pharmacol Physiol. 1996 May;23(5):375-8. doi: 10.1111/j.1440-1681.1996.tb02744.x.

A patient with severe hypertension was found to have mildly impaired 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) activity on the basis of urinary steroid metabolite ratios, low plasma aldosterone, angiotensin II and renin levels and marginally low levels of plasma potassium. 2. The patient also had a compulsively high salt intake. 3. We tested the hypothesis that high salt intake may affect 11 beta-HSD activity. 4. High salt intake in normal subjects did not significantly alter either blood pressure or 11 beta-HSD activity. 5. We suggest that the potentially small hypertensive effect of the partial enzyme deficiency in our patient, also reported in patients with essential hypertension, has been markedly amplified by the very high salt intake.

一名重度高血压患者，基于尿类固醇代谢物比率、低血浆醛固酮、血管紧张素II和肾素水平以及略低的血浆钾水平，发现其11β-羟类固醇脱氢酶（11β-HSD）活性轻度受损。2. 该患者还存在强迫性高盐摄入情况。3. 我们检验了高盐摄入可能影响11β-HSD活性这一假说。4. 正常受试者高盐摄入并未显著改变血压或11β-HSD活性。5. 我们认为，我们的患者中部分酶缺乏潜在的轻微高血压效应（原发性高血压患者中也有报道），已被极高的盐摄入显著放大。

Ingram M C, Wallace A M, Collier A, Fraser R, Connell J M

MRC Blood Pressure Unit, Western Infirmary, Glasgow, Scotland.

Clin Exp Pharmacol Physiol. 1996 May;23(5):375-8. doi: 10.1111/j.1440-1681.1996.tb02744.x.

A patient with severe hypertension was found to have mildly impaired 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) activity on the basis of urinary steroid metabolite ratios, low plasma aldosterone, angiotensin II and renin levels and marginally low levels of plasma potassium. 2. The patient also had a compulsively high salt intake. 3. We tested the hypothesis that high salt intake may affect 11 beta-HSD activity. 4. High salt intake in normal subjects did not significantly alter either blood pressure or 11 beta-HSD activity. 5. We suggest that the potentially small hypertensive effect of the partial enzyme deficiency in our patient, also reported in patients with essential hypertension, has been markedly amplified by the very high salt intake.

一名重度高血压患者，基于尿类固醇代谢物比率、低血浆醛固酮、血管紧张素II和肾素水平以及略低的血浆钾水平，发现其11β-羟类固醇脱氢酶（11β-HSD）活性轻度受损。2. 该患者还存在强迫性高盐摄入情况。3. 我们检验了高盐摄入可能影响11β-HSD活性这一假说。4. 正常受试者高盐摄入并未显著改变血压或11β-HSD活性。5. 我们认为，我们的患者中部分酶缺乏潜在的轻微高血压效应（原发性高血压患者中也有报道），已被极高的盐摄入显著放大。