Cardiovascular regulation after destruction of the C1 cell group of the rostral ventrolateral medulla in rats.

To evaluate the role of C1 neurons in the rostral ventrolateral medulla (RVLM) in cardiovascular regulation, we studied rats in which this cell group was destroyed by the injection of anti-dopamine-beta-hydroxylase-saporin into the RVLM. These immunotoxin injections resulted in 32-99% depletion of the RVLM-C1 neurons and approximately 50% depletion of the A5 cell population. In conscious rats with large (>80%) depletion of the RVLM-C1 cell population, resting arterial pressure was approximately 10 mmHg lower than in control injected rats, although heart rate was not significantly different. Similar results were observed when arterial pressure was recorded in urethan-anesthetized rats, although under anesthesia, heart rate was also reduced in rats with large (>80%) depletion of the RVLM-C1 neuronal population. Sympathoexcitatory responses to baroreceptor unloading, chemoreceptor activation, and electrical stimulation of sciatic nerve afferent fibers were attenuated in rats with >80% depletion of the RVLM-C1 cell population. These effects of RVLM-C1 plus A5 cell populations were not mimicked by either smaller lesions of the RVLM-C1 population or by selective destruction of the A5 cell population with 6-hydroxydopamine. Sympathoinhibitory responses such as decreases in arterial pressure and heart rate evoked by injection of GABA into the RVLM or by intravenous phenylbiguanide administration were not altered by RVLM-C1 plus A5 cell depletion. These data suggest that RVLM-C1 cells contribute to the maintenance of baseline arterial pressure and play an integral role in sympathoexcitatory responses.