Kantaria N, Pantsulaia I, Andronikashvili I, Simonia G
Tbilisi State Medical University Department of Internal Medicine, Georgia.
Georgian Med News. 2016 Sep(258):28-32.
It has been known that salt-sensitivity of blood pressure is defined genetically as well as can be developed secondary to either decreased renal function or by influence of other environmental factors. The aim of the study was to evaluate the possible mechanism for the development of salt-sensitive essential hypertension in the population of Georgia. The Case-Control study included 185 subjects, 94 cases with Essential Hypertension stage I (JNC7) without prior antihypertensive treatment, and 91 controls. Salt-sensitivity test was used to divide both case and control groups into salt-sensitive (n=112) and salt-resistant (n=73) subgroups. Endogenous cardiotonic steroids, sodium and PRA were measured in blood and urine samples at the different sodium conditions. Determinations of circulating levels of endogenous sodium pump inhibitors and PRA were carried out using the ELISA and RIA methods. Descriptive statistics were used to analyze the data. Differences in variables between sodium conditions were assessed using paired t-tests. Salt-sensitivity was found in 60.5% of total population investigated, with higher frequency in females. Salt-sensitivity positively correlated with age in females (r=0.262, p<0.01). Statistically significant positive correlation was found between 24 hour urine sodium concentration changes and salt-sensitivity r=0.334, p<0.01. Significant negative correlation was found between salt-sensitivity and PRA. Since no significant correlations were found between BMI and salt-sensitivity, we assume that BMI and salt-sensitivity should be discussed as different independent risk factors for the development of Essential Hypertension. Significant correlation was found between changes in GFR in salt-sensitive cases and controls p<0.01. This can be explained with comparable hyperfiltration of the kidneys at high sodium load and discussed as early sign of hypertensive nephropathy in salt-sensitive individuals. At the high sodium condition Endogenous MBG and OU were high in salt-sensitive subjects compared to salt-resistant. These compounds decreased after low salt diet in salt-sensitive cases as well as controls but remained within the same level in salt-resistant individuals. MBG and OU levels positively correlated with SBP in salt-sensitive individuals but salt-resistant subjects didn't show any changes. Our results support the idea that chronic high sodium loading (>200 mmol) which is typical in traditional Georgian as well as other diets switch those humoral and pathophysiological mechanisms that can lead to the development of certain type of hypertension in salt-sensitive individuals. Salt intake reduction can prevent development of hypertension in salt-sensitive subjects, although hypertension develops in the salt-resistant individuals but by other mechanism such as RAAS.
已知血压的盐敏感性在遗传学上有定义，也可能继发于肾功能下降或受其他环境因素影响而产生。本研究的目的是评估格鲁吉亚人群中盐敏感性原发性高血压发生的可能机制。病例对照研究纳入了185名受试者，94例未经抗高血压治疗的原发性高血压I期（JNC7）患者以及91名对照。采用盐敏感性试验将病例组和对照组均分为盐敏感（n = 112）和盐抵抗（n = 73）亚组。在不同钠条件下，检测血样和尿样中的内源性强心甾体、钠和肾素活性（PRA）。使用ELISA和RIA方法测定内源性钠泵抑制剂和PRA的循环水平。采用描述性统计分析数据。使用配对t检验评估不同钠条件下变量的差异。在所调查的总人口中，60.5%发现有盐敏感性，女性中的发生率更高。女性中盐敏感性与年龄呈正相关（r = 0.262，p < 0.01）。24小时尿钠浓度变化与盐敏感性之间存在统计学显著正相关（r = 0.334，p < 0.01）。盐敏感性与PRA之间存在显著负相关。由于未发现体重指数（BMI）与盐敏感性之间存在显著相关性，我们认为BMI和盐敏感性应作为原发性高血压发生的不同独立危险因素来讨论。在盐敏感病例和对照中，肾小球滤过率（GFR）变化之间存在显著相关性（p < 0.01）。这可以用高钠负荷下肾脏的类似超滤现象来解释，并可作为盐敏感个体高血压肾病的早期迹象来讨论。在高钠条件下，与盐抵抗者相比，盐敏感受试者的内源性中段脑利钠肽（MBG）和鸟型利钠肽（OU）较高。在盐敏感病例和对照中，低盐饮食后这些化合物水平下降，但在盐抵抗个体中保持在相同水平。在盐敏感个体中，MBG和OU水平与收缩压（SBP）呈正相关，但盐抵抗受试者未显示任何变化。我们的结果支持这样一种观点，即传统格鲁吉亚饮食以及其他饮食中典型的慢性高钠负荷（>200 mmol）会改变那些可导致盐敏感个体发生特定类型高血压的体液和病理生理机制。减少盐摄入可预防盐敏感受试者发生高血压，尽管盐抵抗个体也会发生高血压，但通过其他机制，如肾素 - 血管紧张素 - 醛固酮系统（RAAS）。
