Effect of moxonidine on putative sympathetic neurons in the rostral ventrolateral medulla of the rat.

We used an intracellular recording technique in vitro to investigate the effects of moxonidine on neurons in the rostral ventrolateral medulla (RVLM) with electrophysiological properties similar to premotor sympathetic neurons in vivo. These neurons were classified as firing regularly and irregularly, according to previous reports. Moxonidine is a sympathoinhibitory and antihypertensive agent that is thought to be a ligand of α2-adrenergic receptors and imidazoline type-1 receptors in the RVLM. Moxonidine (2–10 µM) was applied to the perfusate on 4 irregularly firing neurons, and 2 regularly firing neurons. Moxonidine (2 µM) produced only minor depolarization in 2 of these neurons. However, on 4 tested neurons, moxonidine (10 µM) elicited a profound inhibitory effect with hyperpolarization (near –20 mV); these neurons practically ceased firing. These changes were partially reversible. The results would indicate that neurons in the RVLM, recorded in vitro and with similar electrophysiological characteristics to a group of neurons previously identified in vivo in the same bulbar region as barosensitive premotor sympathetic neurons, can be modulated by imidazoline-derivative adrenergic agonists. These results could help to understand the hypotensive effects of moxonidine.