Gadolinium administration into vascularly isolated carotid sinus regions suppresses the neural arc of arterial baroreflex function in anesthetized healthy male rats

Background and Purpose: Thearterial baroreflex is a negative feedback system that modulates autonomic nerve activity to stabilize arterial pressure (AP). Evidence suggests that mechanosensitive channels play a crucial role in sensing changes in AP. Gadolinium is a non-selective blocker of mechanosensitive channels. Although gadolinium has been reported to impair mechanoelectrical transduction of carotid sinus nerve activity, the impact of gadolinium in baroreceptors on cardiovascular regulation via arterial baroreflex function has not been fully elucidated. Therefore, the purpose of this study was to determine the effects of gadolinium administration into vascularly isolated carotid sinus regions on arterial baroreflex function using the baroreflex open-loop condition. Methods: In anesthetized healthy male Sprague-Dawley rats (n = 21, body weight: 376 ± 41 g), the bilateral carotid sinus baroreceptors were isolated from the systemic circulation. The isolated carotid sinuses were then filled with saline (control solution) or three different concentrations of gadolinium (10 mM, 25 mM, and 50 mM). The carotid sinus pressure (CSP) was increased stepwise from 60 to 180 mmHg in increments of 20 mmHg per minute to evaluate the open-loop baroreflex function. The AP, renal sympathetic nerve activity (RSNA), and heart rate (HR) responses to the stepwise CSP input were recorded. Results: RSNA was significantly decreased in response to a stepwise increase in CSP in control (n = 11) and 10 mM gadolinium (n = 2) solutions ( P < 0.05). However, the RSNA response to changes in CSP was reduced by both 25 mM (n = 3) and 50 mM (n = 2) gadolinium solutions. Likewise, although a stepwise increase in CSP significantly decreased AP and HR in control (n = 12) and 10 mM gadolinium (n = 4) solutions ( P < 0.05), 25 mM (n = 3) and 50 mM (n = 2) gadolinium solutions mitigated those responses. Conclusion: We demonstrate that administration of higher concentrations (above 25 mM) of gadolinium into the carotid sinus regions strongly suppresses the neural arc of arterial baroreflex function. These findings suggest that mechanosensitive channels in baroreceptors, which can be almost completely inhibited by higher concentrations of gadolinium, play a fundamental role in arterial baroreflex-mediated cardiovascular regulation. This work was supported by NIH R01 HL-151632. 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.