Medicine (Baltimore). 2026 May 1;105(18):e48609. doi: 10.1097/MD.0000000000048609.
ABSTRACT
Hypertensionis one of the leading causes of cardiovascular disease and premature death worldwide, affecting more than 1.2 billion adults, with a significant part living in low- and middle-income countries. Pediatric hypertension is also a growing concern, with an estimated 4.5% of children in the United States affected. The 2024 European Society of Cardiology guidelines provide updated protocols for diagnosing and treating hypertension in adults, while pediatrics diagnosis is based on age and weight-specific percentiles. The renin-angiotensin-aldosterone system plays a crucial role in blood pressure (BP) regulation, with 2 pathways: classical pathway and alternative pathway. classical pathway increases BP and fluid retention, while alternative pathway counteracts these effects. Neuropeptides such as Nesfatin-1 (Nes-1) and Galanin (Gal), along with the endocannabinoid system, also influence BP regulation. The study focused on adolescents with hypertension, obesity, or combination. From the hospital, 128 patients were recruited to the study. Plasma samples were analyzed for Nes-1, Gal, anandamide (AEA), and 2-arachidonoylglycerol levels. The results showed significantly lower levels of Nes-1 and Gal in the obese hypertensive patients (P = .005 and P = .022 respectively) and obesity groups (P = .022 and P = .035 respectively) compared to the controls. AEA levels did not show significant differences, while 2-arachidonoylglycerol levels were tendential to higher concentration in hypertensive patients. The lower concentration of Nes-1 and Gal can be considered as predictive factors of hypertension in obese patients, with Nes-1 negatively correlated with systolic pressure. Endocannabinoid system, through cannabinoid receptors 1, may also influence BP, though its role requires further research. Understanding these systems could improve the management of hypertension, particularly in pediatric populations.
PMID:42065203 | DOI:10.1097/MD.0000000000048609