Inactivation of the rostral CVLM elevated SNA to 214% of control and arterial pressure by 34 mmHg, eliminating baroreceptor reflex inhibition, whereas caudal CVLM inactivation increased SNA to 196% without affecting the reflex.
The study demonstrates anatomic segregation within the CVLM, where the rostral portion is required for baroreceptor reflex function, while the caudal portion limits sympathetic nerve activity and blood pressure independently of the reflex.
The caudal ventrolateral medulla (CVLM) plays a significant role in the regulation of sympathetic nerve activity (SNA) and arterial pressure; however, the use of lesions to examine its role in mediating baroreceptor reflex control of SNA has yielded discrepant results. We hypothesize that this may have arisen from anatomic segregation of neurons within the CVLM that subserve different functions in sympathetic control. Thus we used microinjections of the excitotoxic agent kainic acid (200 pmol in 20 nl) to determine the effects of inactivation of neuronal cell bodies in a rostral and a caudal subregion of the CVLM on SNA, arterial pressure, and baroreceptor reflex function in urethan-anesthetized rats. Interruption of neuronal activity in the rostral CVLM (sites from 0.6 mm caudal to 0.5 mm rostral to the rostral border of the lateral reticular nucleus) elevated SNA (post-kainic acid 214% of control) and arterial pressure (+34 mmHg) and eliminated the inhibition of splanchnic SNA evoked by either aortic nerve stimulation or the pressor response to intravenous norepinephrine. In addition, the cardiac-related component of spontaneous SNA was abolished as judged from post-R wave averages and from power spectral analysis. In contrast, although a similar disruption of neuronal activity in the caudal CVLM (sites 0.0-0.6 mm rostral to the caudal border of the lateral reticular nucleus) produced a comparable increase in spontaneous SNA (post-kainic acid 196% of control) and arterial pressure (+20 mmHg), it was without effect on the ability of the baroreceptor reflex to inhibit SNA, and it enhanced the synchronization of the spontaneous bursts in SNA to the cardiac cycle. Our results suggest an organization of the CVLM in which neurons in its rostral portion are required for an effective baroreceptor reflex, whereas those in the caudal CVLM serve to limit SNA and blood pressure independent of the baroreceptor reflex.
Cravo et al. (Tue,) reported a other. Microinjections of kainic acid into rostral and caudal subregions of the CVLM vs. Control (baseline) was evaluated on Sympathetic nerve activity (SNA) and arterial pressure. Inactivation of the rostral CVLM elevated SNA to 214% of control and arterial pressure by 34 mmHg, eliminating baroreceptor reflex inhibition, whereas caudal CVLM inactivation increased SNA to 196% without affecting the reflex.