Circulating endothelial progenitor cells, Th1/Th2/Th17-related cytokines, and endothelial dysfunction in resistant hypertension. Academic Article uri icon

abstract

  • Introduction A possible link between chronic vascular inflammation and arterial hypertension is now an object of intensive studies. Objective To compare Th1/Th2/Th17 cells-related cytokines, circulating endothelial progenitor cells (EPC), and endothelial function in subjects with resistant arterial hypertension (RAH) and controlled arterial hypertension (CAH). Methods Blood pressure was measured by electronic sphygmomanometer. EPC were identified as CD34 +/ CD133 +/kinase insert domain receptor (KDR) + cells by flow cytometry. Th1/Th2/Th17 cells-related cytokines were identified using the Human Th1/Th2/Th17 Cytokines MultiAnalyte ELISArray Kit. Endothelium-dependent (FMD) vasodilatation of brachial artery was measured by Doppler ultrasound scanning. Results RAH group (n = 20) and CAH group (n = 20) and 17 healthy individuals (control group) were recruited. In the RAH group, lower blood levels of EPC number (42.4 ± 16.7 cells/mL) and EPC% (0.19 ± 0.08%) were observed than in the CAH group (93.1 ± 88.7 cells/mL; P = 0.017; 0.27 ± 0.17; P = 0.036) and control group (68.5 ± 63.6 cells/mL; P < 0.001; 0.28 ± 0.17%; P = 0.003), respectively. Plasma transforming growth factor-β1 levels were significantly higher in the RAH group (1767 ± 364 pg/mL) than in the CAH group (1292 ± 349; P < 0.001) and in control group (1203 ± 419 pg/mL; P < 0.001). In the RAH group, statistically significant negative correlation was observed between systolic blood pressure and EPC% (r = –0.72, P < 0.01). FMD in the RAH group was significantly lower (5.5 ± 0.8%) than in the CAH group (9.2 ± 1.4; P < 0.001) and in healthy controls (10.1 ± 1.1%; P < 0.001). Conclusions RAH is characterized by reduced circulating EPC, substantial endothelial dysfunction, and increased plasma transforming growth factor-β1 levels.

publication date

  • January 1, 2010