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Exposure to environmentally relevant concentration of second hand smoke increased blood pressure and decreased baroreflex sensitivity in mice
Author(s) -
Pan Shiyue,
Karey Emma,
Chen YiJe,
NievesCintron Madeline,
Pinkerton Kent E,
Chen Chao
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.558.4
Subject(s) - baroreflex , blood pressure , medicine , cardiology , zoology , heart rate , endocrinology , anesthesia , physiology , biology
BACKGROUND Second hand smoke (SHS), a main indoor air pollution, is a significant risk factor for cardiovascular morbidity and mortality. Epidemiological studies link SHS exposure to increased sympathetic nerve activity (SNA) and blood pressure (BP), suggesting a central component in SHS‐induced cardiovascular dysregulation. However, we have limited information on effects of SHS on baroreflex sensitivity (BRS), an indicator of central regulation of BP and a stronger link to cardiovascular morbidity and mortality than the elevated BP. Additionally, we lack information on whether exposure to environmentally relevant levels of SHS affects BP regulation. Here we sought to test the hypothesis that chronic exposure to an environmentally relevant level of SHS elevates BP and reduces BRS. METHODS Adult male C57BL/6J mice (11 wk old) were implanted with BP/ECG telemetry devices. After two weeks of recovery from surgery, mice were randomly assigned to either filtered air (FA, n=18) or SHS (n=14) for up to 12 weeks. The SHS exposure level was similar to that of a smoky bar (3 mg/m 3 , 6 hr/d, 5 d/wk). 36 hours of continuous BP and ECG recordings were performed after the 5 th day of exposure each week. Data were divided into three 12‐hr periods based on light cycle: dark 1, light and dark 2. Standard deviation of beat‐to‐beat BP was taken as the BP variability (BPV). BRS was determined with the sequence method using systolic BP. RESULTS There was no difference in body weight between FA‐ and SHS‐exposed mice over the 12‐wk period. SHS exposure had no effect on dark‐light difference in BP, BPV, and BRS. Comparing to FA mice, SHS mice had higher systolic BP (~2.4 mmHg, p < 0.05), mean BP (~3 mmHg, p <0.05), and diastolic BP (~4 mmHg, p < 0.05) by 4 weeks of exposure. SHS reduced pulse pressure (PP, ~2 mmHg, p < 0.05), although the magnitude of the reduction diminished over time. In contrast, the SHS‐induced reduction in BRS was time dependent and accumulative, having a slower onset than changes in BP and PP, and becoming more severe with increasing exposure duration (−0.8%, −6.2%, and −12.3% for 4, 8, and 12 wk, respectively). SHS did not change BP variability, regardless of exposure duration. CONCLUSIONS The effect of SHS on increased BP was observed after 4 wk of exposure and sustained through 12 wk of exposure. In contrast, SHS‐induced reductions in BRS showed a delayed onset that accumulates with prolonged exposures. The data suggest that SHS may activate multiple mechanisms resulting in BP dysregulation. Support or Funding Information R01 ES025229 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .