The dmNTS is not the source of increased blood pressure variability in baroreflex denervated rats.

A consistent and prominent feature, observed across many species, including our neuromuscular blocked (NMB) rat preparation, is that obliterating the baroafferent inputs to the brainstem, e.g., by sinoaortic denervation (SAD), significantly increases blood pressure variability (BPV). The sources of the BPV, however, are not completely understood, but involve both the central and the peripheral mechanisms. The key central noise source is likely in the brainstem. Previously, in NMB rats, we showed that the maximum gain of the baroreflex system is in the very low frequency (VLF) range of 0.01-0.2 Hz. In this study, using the same NMB preparation, we demonstrated that, after SAD, there was a significant increase in the VLF power of the expiratory systolic blood pressure (EsBP) spectrum, but a decrease in the VLF power of the expiratory heart inter-beat-interval (EIBI) spectrum. Because dmNTS is the only major common anatomic node for the vascular sympathetic and the cardiac parasympathetic pathways, the opposite changes in the post-SAD VLF powers of the EsBP and EIBI spectra suggest that dmNTS is unlikely the major noise source for the post-SAD BPV. Supporting this finding, we found that the dmNTS evoked response to single pulse baroreflex afferent aortic depressor nerve (ADN) stimuli was substantially more reliable than the evoked systolic blood pressure responses to the same stimuli.