You are here:
TRPV1 modulates the cardiovascular and cardiopulmonary response to acute heat exposures in mice
Citation:
Fiamingo, M., L. Klein, M. Vaziri, W. Oshiro, Q. Krantz, P. Evansky, Matthew Gilmour, A. Farraj, AND M. Hazari. TRPV1 modulates the cardiovascular and cardiopulmonary response to acute heat exposures in mice. Visiting Pulmonary Scholar Symposium, Chapel Hill, NC, May 08, 2024.
Impact/Purpose:
This work provides mechanistic insight and biological plausibility into the effects of extreme heat on cardiopulmonary health. It describes the role of TRPV1 and the potential modifying effects of non-chemical stressors.
Description:
Background: Extreme heat events from climate change are classified as the leading cause of weather-related death in the United States and are associated with cardiovascular morbidity and mortality. Potential synergistic effects of housing (ie. psychosocial stress) with extreme heat remain understudied, and transient receptor potential vanilloid 1 (TRPV1), a calcium ion receptor that is activated at high temperatures, remains understudied, might be modulating these responses. Methods: Female C57BL/6J and TRPV1 (-/-) mice were randomly split into either enriched (EH) or depleted housing (DH) for 20 weeks before being exposed to either a normal temperature (NT) control or acute high heat (100°F) (HT) for 1 hour over 3 consecutive days. Immediately following the exposures, WBP was assessed, and HF-echo was conducted 24-hrs later, followed by plasma and tissue collection. Immediately following the exposures, whole body plethysmography was assessed, and high-frequency echocardiography was conducted 24-hrs later, followed by plasma and tissue collection. Results: C57BL6/J EH HT mice had significant decreases in breathing frequency (f), peak inspiratory flow (PIF) and tidal volume (TV), and an increase in enhanced pause (PenH), compared to temperature-matched controls (DH HT). Following the third day of heat exposures, C57BL6/J DH HT mice showed decreased cardiac output (CO) and stroke volume (SV), and increased in heart rate (HR) in both NT and HT EH mice. Ventilatory and cardiac changes were mitigated in TRPV1 (-/-) mice. Conclusions: Enriched housed mice exposed to high heat exhibit the largest changes in ventilation patterns, likely as a result of increased exercise. Depleted housed mice exposed to acute high heat might have worsened cardiovascular outcomes following the exposures. Both ventilatory and cardiovascular adverse outcomes might be mitigated inTRPV1 (-/-) mice. Our findings represent a novel interaction between daily stressors (ie. housing, heat) that might cause long-lasting physiological changes, with TRPV1 potentially acting as a mediator of these responses. (This abstract does not reflect EPA policy.)