Cottone S, Mangano M T, Fulantelli M A, Cerasola G, Salerno L, Nardi E, Lodato G, Traina C
Hypertension Center, University of Palermo, Italy.
Clin Ther. 1989 Jul-Aug;11(4):511-20.
Malignant hypertension developed in an 18-year-old man whose primary hypertension had been diagnosed by chance. Standing blood pressure was 290/170 mmHg. Tests of renal function revealed high blood urea nitrogen and creatinine levels and low levels of both effective renal plasma flow and the glomerular filtration rate. Plasma renin activity and levels of angiotensin II and aldosterone were greatly elevated. Severe concentric left ventricular hypertrophy was noted. The patient received standard antihypertensive treatment with furosemide, propranolol, nifedipine, and prazosin, but his blood pressure did not decrease and there was no improvement in the clinical or biochemical measures. The patient was then given 20 mg of enalapril daily for one year. The inhibition of angiotensin converting enzyme immediately reduced blood pressure. Angiotensin II and aldosterone levels became normal, kidney function and hemodynamics improved, and echocardiograms revealed that the left ventricular hypertrophy had regressed. The results confirm the pathogenetic role of angiotensin II in the development of the malignant phase of hypertension.
一名18岁男性患上恶性高血压,其原发性高血压是偶然被诊断出来的。站立位血压为290/170 mmHg。肾功能检查显示血尿素氮和肌酐水平升高,有效肾血浆流量和肾小球滤过率降低。血浆肾素活性以及血管紧张素II和醛固酮水平大幅升高。发现有严重的同心性左心室肥厚。患者接受了呋塞米、普萘洛尔、硝苯地平和哌唑嗪的标准抗高血压治疗,但血压未下降,临床及生化指标也未改善。随后该患者每天服用20 mg依那普利,持续一年。血管紧张素转换酶的抑制立即降低了血压。血管紧张素II和醛固酮水平恢复正常,肾功能和血流动力学得到改善,超声心动图显示左心室肥厚已消退。这些结果证实了血管紧张素II在高血压恶性阶段发展中的致病作用。