Key result
The authors propose an expanded perspective emphasizing how BPH and OSA disrupt circadian regulation, nocturnal blood pressure dipping, and urine production in patients with nocturia.
Benign prostatic hyperplasia and obstructive sleep apnea may disrupt the suprachiasmatic nucleus, leading to dysregulated ADH secretion and impaired blood pressure dipping, thereby exacerbating the vicious cycle of nocturia and nocturnal hypertension.
We read with great interest the recent article by Nagai et al. discussing the vicious cycle between nocturia and sleep blood pressure regulation [ 1 ]. Their hypothesis regarding atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) as central mediators of nocturia and nocturnal hypertension is insightful. However, we propose an expanded perspective that integrates both urological and sleep medicine viewpoints, emphasizing the roles of benign prostatic hyperplasia (BPH) and obstructive sleep apnea (OSA) in disrupting the suprachiasmatic nucleus (SCN) and its downstream effects on nocturnal blood pressure and urine production. Kato et al. demonstrated that nocturnal polyuria (NP) is significantly associated with attenuated nocturnal systolic blood pressure dipping [ 2 ], reinforcing Nagai et al.’s hypothesis that nocturia is not merely a urological symptom but also a cardiovascular concern. Similarly, Pinilla et al. confirmed that patients with OSA exhibit nondipping blood pressure patterns due to autonomic dysregulation [ 3 ]. These findings suggest that nocturia, hypertension, and OSA are interconnected beyond the cardiac volume overload hypothesis.
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Lin et al. (2025) conducted a letter in Nocturia, benign prostatic hyperplasia, and obstructive sleep apnea. The authors propose an expanded perspective emphasizing how BPH and OSA disrupt circadian regulation, nocturnal blood pressure dipping, and urine production in patients with nocturia.
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