The role of nitric oxide in hypertensive target organ damage in patients without renal impairment: insights from left ventricular global longitudinal strain and albuminuria

Hypertension (HT) is a prevalent chronic condition that contributes significantly to morbidity and mortality by leading to target organ damage. Although nitric oxide (NO) underpins endothelial function and has been implicated in several cardiovascular conditions, its association with subclinical hypertension-mediated organ damage remains unclear. This study aimed to investigate the relationship between nitrite/nitrate (NOx)—an indirect index of NO pathways and subclinical myocardial and renal dysfunction in patients with HT. This study prospectively screened 433 adult hypertensive patients, of whom 400 were included in a cross-sectional analysis after exclusion of conditions potentially confounding cardiac or renal assessment, including end-stage renal disease requiring dialysis. All participants underwent transthoracic echocardiography to assess ventricle functions using left ventricular global longitudinal strain (LV-GLS) and provided a spot urine sample for the measurement of the urine albumin/creatinine ratio (UACR). In addition to NOx levels, inducible and endothelial nitric oxide synthase levels were evaluated from participants’ blood samples. NOx levels were significantly associated with reduced LV-GLS and higher UACR values. In multivariate analysis, lower NOx levels were independently associated with impaired LV-GLS (OR: 0.817; 95% CI: 0.783–0.853; p < 0.001) and albuminuria (OR: 0.905; 95% CI: 0.877–0.934; p < 0.001). NOx may represent an independent biochemical parameter associated with subclinical myocardial and renal dysfunction in patients with HT.