Sympathetic Function During Whole‐Body Cooling is Altered in Hypertensive Adults

Abstract

Acute cold exposure activates the sympathetic nervous system and elicits a robust systemic pressor response. In hypertensive adults (HTN), cardiovascular‐related morbidity and mortality peak during cold winter months; however, the mechanisms underlying this association are not well defined. We hypothesized that whole‐body cold stress would evoke exaggerated increases in muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in HTN compared to normotensive adults (NTN). MSNA (peroneal microneurography), beat‐to‐beat BP (Finometer), and heart rate (HR; ECG) were measured continuously in 10 NTN (6 M/4 W; age 53±3 yrs; resting BP 125±3/79±1 mmHg) and 10 HTN (5 M/5 W; age 57±2 yrs; resting BP 149±6/88±3 mmHg) during whole‐body cooling‐induced reductions in mean skin temperature (Tsk; water‐perfused suit) from 34.0 to 30.5°C. MSNA at 34.0°C was not different between groups (NTN: 51±4 v. HTN: 54±5 bursts· (100 heartbeats)−1; P=0.71). During cooling, the increase in MSNA was exaggerated in HTN (NTN: Δ = 8±3, HTN: Δ = 19±3 bursts· (100 heartbeats)−1; P=0.02). The cooling‐induced increases in both systolic BP (NTN: 9±3, HTN: 19±3 mmHg; P=0.03) and mean arterial pressure (NTN: 6±2, HTN: 10±2 mmHg; P=0.08) were greater in HTN. The HR response to cooling was not different between groups (P=0.16). The slope of the relation between MSNA burst incidence and diastolic BP did not change during cold stress in NTN (Tsk = 34.0°C: ‐4.0±0.7 v. Tsk = 30.5°C: ‐5.0±0.3 bursts· (100 heartbeats)−1·mmHg−1; P=0.17) but increased in HTN (Tsk = 34.0°C: ‐2.9±0.5, Tsk = 30.5°C: ‐5.0±0.4 bursts· (100 heartbeats)−1·mmHg−1; P=0.04). These data demonstrate that the whole‐body cooling‐induced increases in MSNA and BP are augmented in HTN. Further, sympathetic baroreflex sensitivity increases during cooling in HTN, but not NTN, presumably to allow for baroreflex‐mediated buffering of excessive cooling‐induced increases in BP. Collectively, these findings suggest that sympathetic function during cold stress is altered in human hypertension, likely contributing to increased cold‐associated cardiovascular risk.Support or Funding InformationHL093238 (LMA) and HL120471 (JLG)