Qiufang Lian

Evolution of blood pressure from adolescents to youth in salt sensitivies: a 18-year follow-up study in Hanzhong children cohort

BackgroundEssential hypertension mostly originates from children. Salt Sensitivity (SS) is regarded as the intermediate phenotype of essential hypertension. The present study investigated the effects of salt-sensitivity on evolution of blood pressure (BP) and development to hypertension from adolescents to youth.MethodsA baseline survey was carried out in 4,623 adolescents aged 6-15 years old in Hanzhong rural areas in 1987, 310 of whom(mean 9.2 years) were randomly recruited for determination of salt sensitivity using the tests of oral saline load and furosemide sodium-volume depletion. SS was diagnosed in 101 subjects while 209 were determined as non-salt-sensitive (NSS). We made a 18-year followed-up of the cohort in 2005.ResultsThe response rate for surviving baseline adolescents was 71.9%. At follow up, BP in youth with baseline SS was higher than that in NSS (SBP:122.9 ± 13.1 VS 117.3 ± 12.4, P < 0.01; DBP: 78.2 ± 10.4 VS 74.7 ± 10.8, P < 0.05). Longitudinal analysis of 18-year BP evolution, subjects in SS had greater Systolic BP change than subjects in NSS(19.6 ± 12.714.7 ± 12.2, P < 0.01). The incidence of hypertension in salt sensitive group was higher than that in NSS group (15.5% VS 6.3%, RR = 2.34, P < 0.05).ConclusionOur findings indicate that adolescents with higher BP salt-sensitivity have a higher rate of incident hypertension in youth. Salt sensitivity could be at high risk predisposing to development of hypertension from adolescents to youth.

Involvement of the lymphatic system in salt-sensitive hypertension in humans

Summary Background The mechanisms of salt sensitivity as an important intermediate phenotype of essential hypertension remain elusive. A novel theory proposes that lymphatic vessels regulate sodium and fluid homeostasis. Since vascular endothelial growth factor C (VEGF-C) plays a vital role in lymphatic capillary hyperplasia, we hypothesized that VEGF-C was involved in salt-sensitive hypertension. We therefore investigated its plasma concentration in salt-sensitive subjects. Material/Methods Twenty-seven subjects (BP ≤160/100 mmHg; age range 25–50 years) from a rural community of northern China were enrolled in this study. The baseline BP of volunteers was monitored for 3 days, followed by a low-salt diet for 7 days (3 g/day, NaCl) and a high-salt diet for 7 days (18 g/day, NaCl). Those who exhibited a BP increase of 10% from low-salt period to high-salt period were diagnosed as salt-sensitive subjects. The concentration of plasma VEGF-C was measured by an immunoenzyme method (ELISA). Result High salt intake significantly increased the plasma VEGF-C level. It was higher in the salt-sensitive subjects (3642.2±406.1 pg/ml) than in the salt-resistant subjects (2249.8±214.6 pg/ml). The comparison of VEGF-C levels between the 2 groups had significant statistical difference (P<0.01). Conclusions The VEGF-C level increases significantly in the salt-sensitive subjects after high salt intake. VEGF-C could be used as a biomarker of salt sensitivity.

Lack of Family-Based Association between Common Variations in WNK1 and Blood Pressure Level

Background WNK1 (With No-lysine Kinase 1) modulates numerous sodium transport-related ion channels involved in regulation of blood pressure. Several studies have indicated associations between the common variants of the WNK1 gene and hypertension or blood pressure levels. However, little data exists on Asian populations and normotensive or pre-hypertensive subjects. Our aim was to detect whether the common variations in the WNK1 gene are potential contributors to individual variations in blood pressure in a family-based sample. Material/Methods 525 individuals from 116 families were selected from a rural community of Northern China. Five single-nucleotide polymorphisms were selected from the WNK1 gene. Single-marker and haplotype analyses were conducted using the Family-Based Association Test program. Results Regretful, no associations for the 5 WNK1 SNPs and the constructed haplotype blocks of WNK1 with blood pressure level reached nominal statistical significance. Conclusions We conclude that although multiple candidate genes are involved in development of hypertension, the genetic polymorphism in WNK1 is not a major contributor to the observed variability in blood pressure and familial clustering risk of hypertension.

INFLUENCE OF SALT LOADING AND POTASSIUM SUPPLEMENT ON SHORT TERM BLOOD PRESSURE VARIABILITY FOR SALT-SENSITIVITY ADULTS

Objectives To observe the change of short blood pressure variation on salt-sensitive normotensive people after sodium-potassium diet, and explore the relationship between blood pressure variability and salt-sensitivity. Methods A baseline survey was carried out in 93 normotensive adults (age>16) in Mei county, Shanxi province from April to October, 2004. All subjects were recruited and sequentially maintained on a protocol with 7 days low salt diet, 7 days high salt diet, and high salt diet with potassium supplementation for another 7 days. We measured blood pressure three times on the last day of each stage, and compute the SD and coefficient of variation as indicator of short term blood pressure variability. Results Completed a total of 93 cases, 32.26% for the salt sensitivity. Baseline blood pressure variability of salt-sensitive was larger than salt-resistive group, and there was significant difference on systolic pressure. Salt restriction and potassium supplementation reduced short-term blood pressure variability of salt-sensitivity, while high-salt diet increased blood pressure variation, whereas no obvious changes were observed in non-salt-sensitive group. Conclusions High salt intake and salt sensitivity are important risk factors for increasing blood pressure variation. Salt restriction and potassium supplementation may be protective.

HIGH SALT INTAKE FAIL TO ENHANCE PLASMA ADIPONECTIN IN NORMOTENSIVE SALT-SENSITIVE SUBJECTS

Objectives Evidences show that salt could modulate adiponectin and inflammation level in normal individuals. Therefore, we hypothesised that abnormalities of adiponectin and inflammation may be the potential mechanism of salt sensitivity. Aims of the study were to investigate whether different alteration of adiponectin and inflammation level in response of high salt were exhibited between normotensive salt sensitive and salt resistant subjects. Methods 30 normotensive subjects (aged 25–50 years) were selected from a rural community of Northern China. All of the people were sequentially maintained on 3 days baseline investigate, a low-salt diet for 7 days (3 g/day, NaCl), then a high-salt diet for 7 days (18 g/day). Salt-sensitivity was diagnosed in 10 subjects who exhibited a response of the increase in mean BP by ≥10% from low-salt period to high-salt period. Total adiponectin was determined using a validated sandwich ELISA employing an adiponectin-specific antibody. Results There was no difference of plasma adiponectin between normotensive salt sensitive subjects and normotensive salt resistant subjects during any salt intake. However, plasma adiponectin higher significantly in high salt intake in normotensive salt resistant subjects than low salt diet (6.1±1.3 vs 7.1±1.7 µg/ml, p=0.047). However, high salt intake could not affect adiponection in normotensive salt sensitive subjects (6.4±2 vs 5.9±2.1 µg/ml, p=0.481). Conclusions Our data indicates that the disturbance of adiponectin exists in normotensive salt sensitive subjects during high salt diet, which may be a novel underlying mechanism of salt sensitivity.