Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, University of the Witwatersrand Medical School, 7 York Rd, Parktown, 2193 Johannesburg, South Africa.
Hypertension. 2012 Jan;59(1):62-9. doi: 10.1161/HYPERTENSIONAHA.111.181230. Epub 2011 Dec 5.
In high-Na(+), low-K(+) diets, which suppress renin release in salt-sensitive groups, the mechanisms maintaining increases in renin-angiotensin-aldosterone system activation downstream from renin and renin-angiotensin-aldosterone system-induced effects on blood pressure (BP) are uncertain. Whether circulating angiotensinogen concentrations (AGT) or its determinants may contribute to maintaining serum aldosterone concentrations (aldosterone) and increases in BP on high-Na(+), low-K(+) diets was evaluated in 579 participants of a community sample of African ancestry. Plasma renin concentrations were inversely related to BP (P<0.0001) and an index of salt intake (24-hour urinary Na(+)/K(+), P<0.0001). An interaction between AGT and urinary Na(+)/K(+) was independently associated with aldosterone (P<0.001) and systolic BP (SBP; P<0.05). Independent of confounders, in participants with urinary Na(+)/K(+) at or more than the median for the sample, AGT was positively associated with aldosterone (P<0.0001) and SBP (P<0.005). No independent AGT-aldosterone or AGT-SBP relationships were noted in participants with urinary Na(+)/K(+) less than the median for the sample. Standardized β-coefficients (slopes) of AGT-aldosterone and AGT-SBP relationships were greater in participants with urinary Na(+)/K(+) at or more than the median (AGT-aldosterone=0.30±0.06, AGT-SBP=0.16±0.05) compared with those with urinary Na(+)/K(+) less than the median (AGT-aldosterone=-0.04±0.06; AGT-SBP=-0.03±0.05; P<0.01-0.0001 for comparison of slopes). The AGT-SBP relationship in participants with urinary Na(+)/K(+) at or more than the median for the sample was equivalent to the relationship between body mass index and BP. In conclusion, in participants of African ancestry, in the presence of high-Na(+), low-K(+) diets, which suppress renin release, renin-angiotensin-aldosterone system activation and its impact on BP are maintained in part by AGT.
在高钠(+)、低钾(+)饮食中,这种饮食抑制了盐敏感人群肾素的释放,因此,维持肾素-血管紧张素-醛固酮系统(renin-angiotensin-aldosterone system,RAAS)激活以及 RAAS 对血压(blood pressure,BP)影响的机制尚不清楚。在一个非裔人群的社区样本中,579 名参与者接受了高钠(+)、低钾(+)饮食,评估了循环血管紧张素原浓度(angiotensinogen concentration,AGT)或其决定因素是否有助于维持血清醛固酮浓度(aldosterone)和升高的血压。血浆肾素浓度与 BP(P<0.0001)和盐摄入量指数(24 小时尿钠(+)/钾(+),P<0.0001)呈负相关。AGT 与尿钠(+)/钾(+)之间的相互作用与醛固酮(P<0.001)和收缩压(systolic blood pressure,SBP;P<0.05)独立相关。在尿钠(+)/钾(+)处于或高于样本中位数的参与者中,独立于混杂因素,AGT 与醛固酮(P<0.0001)和 SBP(P<0.005)呈正相关。在尿钠(+)/钾(+)低于样本中位数的参与者中,未观察到 AGT-醛固酮或 AGT-SBP 之间的独立关系。在尿钠(+)/钾(+)处于或高于中位数的参与者中,AGT-醛固酮和 AGT-SBP 关系的标准化β系数(斜率)较大(AGT-醛固酮=0.30±0.06,AGT-SBP=0.16±0.05),而尿钠(+)/钾(+)低于中位数的参与者的斜率较小(AGT-醛固酮=-0.04±0.06;AGT-SBP=-0.03±0.05;P<0.01-0.0001 比较斜率)。在样本中尿钠(+)/钾(+)处于或高于中位数的参与者中,AGT-SBP 与 BMI 和 BP 之间的关系相当。结论:在非裔人群中,在高钠(+)、低钾(+)饮食抑制肾素释放的情况下,肾素-血管紧张素-醛固酮系统的激活及其对血压的影响部分是由 AGT 维持的。