Hemorrhage initially triggers a rise in sympathetic nerve activity (SNA) that maintains blood pressure (BP); however, SNA is suppressed following severe blood loss causing hypotension. We hypothesized that adrenergic C1 neurons in the rostral ventrolateral medulla (C1) drive the increase in SNA during compensated hemorrhage, and a reduction in C1 contributes to hypotension during decompensated hemorrhage. Using fiber photometry, we demonstrate that C1 activity increases during compensated hemorrhage and falls at the onset of decompensated hemorrhage. Using optogenetics combined with direct recordings of SNA, we show that C1 activation mediates the rise in SNA and contributes to BP stability during compensated hemorrhage, whereas a suppression of C1 activity is associated with cardiovascular collapse during decompensated hemorrhage. Notably, re-activating C1 during decompensated hemorrhage restores BP to normal levels. In conclusion, C1 neurons are a nodal point for the sympathetic response to blood loss.
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| http://dx.doi.org/10.1016/j.celrep.2022.110480 | DOI Listing |
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