Key result
Low nocturnal melatonin links to a ~6 mmHg greater MAP increase during high-salt loading.
Why the study?
Salt-sensitive hypertension is more common in metabolic syndrome, but the underlying biological mechanisms remain poorly understood, including the role of reduced nocturnal melatonin.
Is reduced night-time melatonin production associated with salt sensitivity and altered BP circadian rhythm in adults with metabolic syndrome and untreated hypertension?
Observational (n=130)
Is reduced night-time melatonin production associated with salt sensitivity and altered BP circadian rhythm in adults with metabolic syndrome and untreated hypertension?
Reduced night-time melatonin secretion is associated with increased salt sensitivity and non-dipping blood pressure patterns in adults with metabolic syndrome and untreated hypertension.
Low melatonin may mark salt sensitivity in metabolic syndrome hypertension; leaves open causal role and therapeutic implications.
Objective: Salt-sensitive hypertension is more common among metabolic syndrome (MetS) patients. However, the biological mechanisms behind this phenomenon remain poorly understood. Melatonin, a regulator of circadian rhythms and nocturnal blood pressure (BP) decline, may influence kidney sodium reabsorption and vascular tone. We aimed to determine whether reduced night-time melatonin production is related to salt sensitivity and BP circadian rhythm in adults with MetS. Design and method: We investigated 130 adults with MetS and untreated hypertension. All subjects were tested for salt sensitivity using a modified Sullivan protocol. BP circadian rhythm was assessed by 24-hour ambulatory blood pressure monitoring. Nocturnal melatonin secretion was estimated from the first morning urine using urinary 6-sulfatoxymelatonin (aMT6 s), normalized to creatinine (aMT6 s/Cr). Plasma renin activity, aldosterone, metabolic parameters, and renal function markers were also evaluated. Results: Salt sensitivity was present in 82 of 130 patients (63.1%). Patients with low urinary aMT6 s/Cr had a mean arterial pressure increase of 15.2 mmHg (SD 4.5) during the high-salt phase. Patients with higher aMT6 s/Cr levels had a mean arterial pressure increase of 9.4 mmHg (SD 3.7). Low aMT6 s/Cr levels were associated with more frequent non-dipping patterns and greater nighttime systolic load. In multivariate analysis, aMT6 s/Cr remained a significant predictor after adjustment for age, central obesity, metabolic parameters, aldosterone, and estimated glomerular filtration rate. Conclusions: Reduced night-time melatonin secretion appears to be an important biological factor contributing to salt-sensitive hypertension in MetS. Lower melatonin production may impair the circadian regulation of vascular tone and renal sodium handling, leading to non-dipping patterns and increased 24-hour BP load. Circadian biomarkers such as aMT6 s/Cr may improve risk stratification, and interventions aiming to restore melatonin rhythms could represent an additional strategy in the management of salt-sensitive hypertension in MetS.
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Andronikashvili et al. (2026) conducted an observational in Metabolic syndrome and untreated hypertension (n=130). Low nocturnal melatonin secretion vs. Higher nocturnal melatonin secretion was evaluated on Mean arterial pressure increase during the high-salt phase. Low nocturnal melatonin secretion was associated with a greater mean arterial pressure increase during high-salt loading (15.2 vs 9.4 mmHg) in adults with metabolic syndrome and untreated hypertension.
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