Chronic Stress Augments the Cardiogenic Sympathetic Afferent Reflex in Sprague-Dawley Rats

Background: Chronic psychological stress increases sympathetic nervous system activity and is a well-known risk factor for hypertension and cardiovascular diseases. Myocardial ischemia leads to the release of ischemic metabolites, one of which is bradykinin, which stimulates cardiac afferents, causing sympathetic excitation and chest pain. This response is referred to as the cardiogenic sympathetic afferent reflex (CSAR) and is characterized by a sympathetically mediated increase in blood pressure. Although the CSAR may preserve cardiac perfusion, it also increases cardiac workload and can worsen ischemic injury. Disorders such as Post Traumatic Stress Disorder, Generalized Anxiety Disorder, and Major Depressive Disorder are associated with chronically elevated sympathetic activity and cardiovascular dysfunction. However, the effect on the CSAR is not known. Therefore, in this study, we tested the hypothesis that chronic foot shock stress augments the CSAR in Sprague-Dawley rats. Methods: Sixteen Sprague-Dawley rats were used. The experimental group (N=8 total rats: N=4 males and N=4 females) were conditioned with two-hour bouts of foot shock twice daily for fifteen consecutive days. Control rats (N=8 total rats: N=4 males and N=4 females) were not administered foot shock. Following conditioning, we anesthetized the rats and measured heart rate (HR), blood pressure (BP), and renal sympathetic nerve activity (RSNA) during baseline and the reflex response to epicardial bradykinin (10 µg/ml). Results: Rats administered foot shock stress exhibited a significantly (p < 0.05) elevated baseline BP (112±4.4mmHg) and RSNA (0.0052±0.009µV) compared with controls (BP: 87±3.0mmHg, & RSNA: 0.024±0.004µV). Epicardial bradykinin in the experimental group elicited a significant (p < 0.05) increase in BP (147±3.9mmHg) and RSNA (0.103±0.014µV), and this response was significantly greater than that of the controls (BP: 131±4.9mmHg, & RSNA: 0.071±0.009µV). Neither the mean baseline HR nor the mean reflex tachycardia was significantly different in the control group compared with the foot shock-treated group. Conclusions: Chronic stress has been shown to increase basal cardiovascular-related sympathetic activity and augment the CSAR. The findings from this study advance our understanding of the link between chronic stress and the potential to augment myocardial ischemia. However, the central pathways and mechanisms remain unknown. This ongoing scientific discourse invites further research in this crucial area. NIH HL145645 01 and HL147286-01 to M. R. Zahner. We would like to acknowledge Dr. Justin Gass and Dr. Liza Wills for the generous use of their behavioral equipment. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.