Doulton Timothy W, Saggar-Malik Anand K, He Feng J, Carney Christine, Markandu Nirmala D, Sagnella Guiseppe A, MacGregor Graham A
Blood Pressure Unit, Department of Cardiac and Vascular Sciences, UK.
J Hypertens. 2006 May;24(5):939-45. doi: 10.1097/01.hjh.0000222765.30348.0d.
It has been suggested that inappropriate stimulation of the renin-angiotensin system (RAS) is responsible for the increase in blood pressure that occurs in autosomal-dominant polycystic kidney disease (ADPKD) before the development of renal failure. However, the interpretation of previous studies in ADPKD patients is confounded by inadequate matching with control populations for blood pressure and renal function, or failure to control the sodium intake of participants.
A double-blind, placebo-controlled study of two different sodium intakes (350 and 50 mmol/day for 5 days) in a group of 11 hypertensive ADPKD patients and eight matched control subjects with essential hypertension. In addition, blood pressure and hormonal responses were measured after the administration of the angiotensin-converting enzyme inhibitor enalapril for 3 days.
Blood pressure and hormonal responses of the RAS after a reduction in sodium intake and after the administration of enalapril were identical in ADPKD patients and controls.
Activation of the classic circulating RAS is no greater in hypertensive ADPKD patients than in individuals with essential hypertension.
有人提出,在常染色体显性遗传性多囊肾病(ADPKD)患者出现肾衰竭之前,肾素 - 血管紧张素系统(RAS)的不适当刺激是导致血压升高的原因。然而,以往对ADPKD患者的研究解读因与对照组在血压和肾功能方面匹配不足,或未能控制参与者的钠摄入量而受到混淆。
对11例高血压ADPKD患者和8例匹配的原发性高血压对照受试者进行双盲、安慰剂对照研究,设置两种不同的钠摄入量(每天350和50 mmol,持续5天)。此外,在给予血管紧张素转换酶抑制剂依那普利3天后测量血压和激素反应。
ADPKD患者和对照组在钠摄入量减少后以及给予依那普利后的血压和RAS激素反应相同。
高血压ADPKD患者中经典循环RAS的激活程度并不高于原发性高血压患者。