Abnormal renin short feedback loop in essential hypertension is reversible with converting enzyme inhibition.
Abnormal renin short feedback loop in essential hypertension is reversible with converting enzyme inhibition.
复制标题
原发性高血压中异常的肾素短反馈环路可通过抑制转化酶而逆转。
DOI：
10.1172/jci110622
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Williams,GH
中科院分区：
文献类型：
--
作者：
LeBoff,Ms;Dluhy,RG;Hollenberg,NK;Moore,TJ;Koletsky,RJ;Williams,GH
血管紧张素II（AII）对肾素释放的抑制（所谓的短反馈回路）在原发性高血压中减弱。为了确定这种异常是否是可逆的，在钠限制性原发性高血压患者和正常对照中评估了肾素释放：（a）在给药不同间隔的卡托普利期间和（B）在输注分级剂量的AII之后（0.3-3 ng/kg/min）在用卡托普利慢性降低血浆AII水平之前和之后（每6小时25-50 mg）持续70 h。在对照受试者中，单次给药后血浆肾素活性（PRA）高于对照组的最大增量（11.9±3 ng/ml/h）显著高于高血压患者（8.1± 1.7ng/ml/h）（P< 0.02），尽管高血压患者AII水平降低相似，舒张压降低显著更大。高血压患者持续服用卡托普利70 h后，PRA高于基线（11.4±2.9 ng/ml/h）升至对照组水平（11±2.6 ng/ml/h）;两组间AII和舒张压下降无显著性差异，与正常血压组相比，AII不能抑制高血压患者的肾素释放，尽管在每种AII剂量下，舒张期血增量显著增加，AII水平相当。此外，比较开搏通治疗前后的下降，在AII水平或舒张压水平相当的情况下，PRA下降幅度更大。最后，AII postcaptopril在高血压患者中对PRA的抑制与正常对照组中所见无明显区别。因此，AII对肾素的调节受损是可逆的，延长卡托普利治疗，这表明这种异常不是由于固定的结构缺陷，而是由于可逆的病变。
The suppression of renin release by angiotensin II (AII) (the so-called short feedback loop) is blunted in essential hypertension. To determine whether this abnormality is reversible, renin release was assessed in sodium-restricted essential hypertensives and normal controls: (a) during the administration of captopril for varying intervals and (b) following the infusion of graded doses of AII (0.3-3 ng/kg per min) before and after plasma levels of AII had been chronically reduced with captopril (25-50 mg every 6 h) for 70 h.In control subjects, the maximal increment above control in plasma renin activity (PRA) after a single dose of captopril (11.9±3 ng/ml per h) was significantly (P< 0.02) greater than in hypertensives (8.1±1.7 ng/ml per h) despite similar reductions in AII levels and significantly greater decrements in diastolic blood pressure in the hypertensives. When captopril was continued for 70 h, the PRA increments above base line in hypertensive subjects (11.4±2.9 ng/ml per h) rose to levels seen in the controls (11±2.6 ng/ml per h); there were no significant differences in the AII or diastolic blood pressure decrements between the two groups.Compared with normotensive subjects, AII failed to suppress renin release in hypertensive subjects despite significantly greater diastolic blood increments and comparable AII levels achieved at each AII dose.After captopril treatment, AII now produced significant declines in PRA in the hypertensives; moreover, comparing declines pre- and postcaptopril, greater PRA decrements were seen either at comparable rises in levels of AII or diastolic blood pressure. Finally, the suppression of PRA by AII postcaptopril in hypertensives was now indistinguishable from that seen in normal controls. Thus, the impaired regulation of renin by AII is reversible with prolonged captopril treatment, suggesting that this abnormality is not due to a fixed structural defect but to a reversible lesion.