Cardiovascular effects of agmatine within the rostral ventrolateral medulla are similar to those of clonidine in anesthetized rats.

Agmatine was isolated from bovine brain in 1994. It exhibits various functions, as a consequence of which it meets the criteria for an endogenous brain neurotransmitter. However, its physiological action on the cardiovascular system remains unclear. This study was designed to clarify its cardiovascular effects when administered into the rostral ventrolateral medulla (RVLM) in anesthetized and paralyzed rats. Unilateral injection of clonidine (5 nmol) into the RVLM significantly decreased mean arterial pressure (MAP) and heart rate (HR). Unilateral injection of agmatine (5 nmol) produced similar effects to clonidine. The amplitude of the decrease in HR was the same as with clonidine, but the amplitude of the decrease in MAP was less pronounced. The cardiovascular inhibition induced by clonidine (5 nmol) and agmatine was abolished by idazoxan (5 nmol). Similar to clonidine, agmatine inhibited the pressor effect of L-glutamate (2 nmol) injected into the RVLM. The duration of this effect (about 6 min) was shorter than that observed with clonidine (about 12 min). Bilateral injection of agmatine into the RVLM inhibited the depressor response induced by baroreflex activation (electrical stimulation of the aortic nerve), and this effect was similar to, but less pronounced than, that induced by clonidine. Idazoxan (5 nmol) antagonized the cardiovascular effects of clonidine and agmatine within the RVLM. However, it produced a similar effect to clonidine injected into the RVLM. It is concluded that agmatine exerts a similar cardiovascular effect to clonidine, with less potency within the RVLM. Idazoxan might be a partial agonist for imidazoline I(1) receptors.