Using Borderline Hypertensive Rats to Study How Post-Traumatic Stress Syndrome Augments the Cardiogenic Sympathetic Afferent Reflex
Abstract
Post Traumatic Stress Disorder (PTSD) is a condition where individuals encounter extreme thoughts or feelings after a traumatic event. This can lead to flashbacks that can significantly impact their physical and mental well-being. PTSD can also increase sympathetic nervous system activity leading to hypertension and increased risk of myocardial ischemia. Increased sympathetic activity can also augment the severity of the cardiogenic sympathetic afferent reflex (CSAR), in which myocardial ischemia activates cardiac nerve endings and increases coronary blood flow. Paradoxically, it also increases the heart's oxygen demand and may expand the locus of ischemic injury. Thus, PTSD not only increases the chances of myocardial ischemia but may also increase mortality. However, the effect of PTSD on this reflex has been largely overlooked. We have recently shown that in Sprague Dawley rats, chronic foot shock stress modeling PTSD augments the CSAR. We also showed that the CSAR is elevated in the spontaneous hypertensive rat, a model of sympathetically mediated hypertension. In this study, we generated a Borderline Hypertensive Rats (BHR) colony. These rats exhibit mildly elevated blood pressure under baseline conditions but experience a sharp, sustained increase when exposed to stress. We exposed BHRs to foot shock stress twice daily for two hours for fifteen consecutive days. After treatment, we measured blood pressure, heart rate, and sympathetic nerve activity and tested the CSAR. We hypothesized that BHRs exposed to chronic stress would show increased blood pressure and heart rate and augmented CSAR compared with unstressed BHRs. Strangely, blood pressure, heart rate, sympathetic nerve activity, or CSAR response in BHRs exposed to chronic stress was no different compared with unstressed BHRs. Our next step is to outfit rats with radiotelemetry devices to measure daily blood pressure and heart rate and increase the intensity of the foot-shock stress to ensure it elicits hypertension.
Start Time
16-4-2025 1:30 PM
End Time
16-4-2025 4:00 PM
Presentation Type
Poster
Presentation Category
Health
Student Type
Undergraduate Student
Faculty Mentor
Matthew Zahner
Faculty Department
Biomedical Health Sciences
Using Borderline Hypertensive Rats to Study How Post-Traumatic Stress Syndrome Augments the Cardiogenic Sympathetic Afferent Reflex
Post Traumatic Stress Disorder (PTSD) is a condition where individuals encounter extreme thoughts or feelings after a traumatic event. This can lead to flashbacks that can significantly impact their physical and mental well-being. PTSD can also increase sympathetic nervous system activity leading to hypertension and increased risk of myocardial ischemia. Increased sympathetic activity can also augment the severity of the cardiogenic sympathetic afferent reflex (CSAR), in which myocardial ischemia activates cardiac nerve endings and increases coronary blood flow. Paradoxically, it also increases the heart's oxygen demand and may expand the locus of ischemic injury. Thus, PTSD not only increases the chances of myocardial ischemia but may also increase mortality. However, the effect of PTSD on this reflex has been largely overlooked. We have recently shown that in Sprague Dawley rats, chronic foot shock stress modeling PTSD augments the CSAR. We also showed that the CSAR is elevated in the spontaneous hypertensive rat, a model of sympathetically mediated hypertension. In this study, we generated a Borderline Hypertensive Rats (BHR) colony. These rats exhibit mildly elevated blood pressure under baseline conditions but experience a sharp, sustained increase when exposed to stress. We exposed BHRs to foot shock stress twice daily for two hours for fifteen consecutive days. After treatment, we measured blood pressure, heart rate, and sympathetic nerve activity and tested the CSAR. We hypothesized that BHRs exposed to chronic stress would show increased blood pressure and heart rate and augmented CSAR compared with unstressed BHRs. Strangely, blood pressure, heart rate, sympathetic nerve activity, or CSAR response in BHRs exposed to chronic stress was no different compared with unstressed BHRs. Our next step is to outfit rats with radiotelemetry devices to measure daily blood pressure and heart rate and increase the intensity of the foot-shock stress to ensure it elicits hypertension.