MicroRNA-133a and MicroRNA-145 May Be Involved in the Development of Hypertension-Mediated Organ Damage in Children with Primary Hypertension—A Preliminary Study

<b>Background/Objectives:</b> Studies in adults have demonstrated the essential role of microRNAs in developing hypertension and their effect on hypertension sequelae. In this preliminary study, we aimed to investigate the expression of five miRNA particles, miRNA-21, miRNA-27a, miRNA-27b, miRNA-133a, and miRNA-145, in school-aged children with primary hypertension and to examine their correlations with blood pressure and arterial and heart properties. <b>Methods:</b> In 22 hypertensive children (15.1 ± 1.9 years), we measured blood pressure parameters (office, central, and 24 h), the urinary albumin/creatinine ratio, and the pulse wave velocity (PWV) before and after one hour of aerobic exercise. The left ventricular mass index (LVMI) and common carotid artery intima-media thickness (cIMT) were also assessed. The relative miRNA expression was calculated using the 2^-ΔΔCt method with miRNA-16 as an endogenous control and the pre-exercise miRNA expression levels as the control (baseline). <b>Results:</b> We found a statistically significant decrease in both the office and 24 h ambulatory diastolic blood pressure after 1 h of exercise (82.2 ± 8.5 mm Hg versus 78.6 ± 8.8 mm Hg, <i>p</i> = 0.01 and 75.0 ± 8.3 mm Hg versus 73.0 ± 7.4 mm Hg, <i>p</i> = 0.02). The increase in miRNA-133a expression after exercise correlated positively with the LVMI. Furthermore, the rise in miRNA-145 expression after exercise correlated negatively with the systolic and diastolic office and 24 h blood pressure and with markers of arterial damage: 24 h PWV and cIMT. <b>Conclusions:</b> In conclusion, miRNA-133a may be a biomarker of left ventricular hypertrophy in children with elevated blood pressure. Additionally, changes in miRNA-145 expression induced by exercise might reduce the blood pressure after exercise and protect against arterial damage. Both miRNA-133a and miRNA-145 may be involved in epigenetic alterations in children affected by primary hypertension that may contribute to the exacerbation of HMOD.