Key result
Standing-induced skin sympathetic nerve activity spikes linked to ~2.7-fold higher odds of nocturnal hypertension.
Why the study?
Are standing-induced changes in skin sympathetic nerve activity (SKNA) associated with orthostatic hypertension and nocturnal hypertension in outpatients with hypertension?
Cross-Sectional (n=141)
Are standing-induced changes in skin sympathetic nerve activity (SKNA) associated with orthostatic hypertension and nocturnal hypertension in outpatients with hypertension?
Greater standing-induced increases in skin sympathetic nerve activity (aSKNA) are associated with nocturnal hypertension, nondipping/riser patterns, and show a trend toward association with orthostatic hypertension, supporting the noninvasive use of SKNA to characterize sympathetic-driven hypertension phenotypes.
SKNA may associate with orthostatic and nocturnal hypertension phenotypes; leaves open its role in risk stratification or management.
Excessive sympathetic activity may contribute to orthostatic hypertension and nocturnal hypertension. However, evidence on associations between skin sympathetic nerve activity (SKNA), assessed noninvasively using neuECG, and these hypertension phenotypes is limited. In this cross-sectional observational study, simultaneous SKNA and supine-to-standing blood pressure (BP) measurements were performed among outpatients with hypertension to examine these associations. Average SKNA (aSKNA) during supine and standing periods, and the percentage change in aSKNA from supine to standing (aSKNA%-changesupine-to-standing) were calculated. Orthostatic hypertension was defined as a supine-to-standing BP increase ≥20/10 mm Hg or conversion from <140/90 mm Hg to ≥140/90 mm Hg. Nighttime home BP was measured for 7 consecutive days; nocturnal hypertension was defined as nighttime BP ≥ 120/70 mm Hg. Associations of SKNA measures with orthostatic and nocturnal hypertension were examined using logistic regression analyses. A total of 141 participants (mean age, 67.6 years; 53.9% men) were included in the analyses. aSKNA%-changesupine-to-standing was correlated with standing SBP (rs = 0.221) and nighttime SBP (rs = 0.280). The adjusted odds ratio (OR) (95% CI) for orthostatic hypertension comparing the highest with the lowest tertile of aSKNA%-changesupine-to-standing was 2.18 (0.89-5.35). The corresponding OR for nocturnal hypertension was 2.74 (1.01-7.41) after adjustment for age and sex, and the corresponding OR for nondipping and riser patterns was 3.70 (1.38-9.90). In the current analysis, greater standing-induced increases in aSKNA tended to be associated with orthostatic and nocturnal hypertension, suggesting the potential role of SKNA in characterizing hypertension phenotypes associated with excessive sympathetic activity.
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Narita et al. (2026) conducted a cross-sectional in Hypertension (n=141). Highest tertile of standing-induced percentage change in average skin sympathetic nerve activity (aSKNA%-change supine-to-standing) vs. Lowest tertile of aSKNA%-change supine-to-standing was evaluated on Nocturnal hypertension (nighttime BP ≥120/70 mm Hg) and orthostatic hypertension (supine-to-standing BP increase ≥20/10 mm Hg or conversion to ≥140/90 mm Hg) (OR 2.74, 95% CI 1.01-7.41). Greater standing-induced increases in skin sympathetic nerve activity were associated with nocturnal hypertension (adjusted OR 2.74; 95% CI 1.01-7.41) and orthostatic hypertension (OR 2.18).
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