Mitogen-Activated Protein Kinase Phosphorylation in the Rostral Ventrolateral Medulla Plays a Key Role in Imidazoline (I1)-Receptor-Mediated Hypotension

摘要: Our previous study showed that rilmenidine, a selective I1-imidazoline receptor agonist, enhanced the phosphorylation of mitogen-activated protein kinase (MAPK)p42/44, via phosphatidylcholine-specific phospholipase C pathway in pheochromocytoma cell line (PC12). In present study, we tested hypothesis enhancement MAPK rostral ventrolateral medulla (RVLM) contributes to hypotensive response elicited by I1-receptor activation vivo. Systemic rilmenidine (600 μg/kg i.v.) hypotension and bradycardia along with significant elevation MAPKp42/44, detected immunohistochemistry, RVLM neurons. To obtain conclusive evidence latter was I1-receptor-mediated, similar responses were intracisternal (i.c.) (25 μg/rat) or highly α2-agonist α-methylnorepinephrine (4 μg/rat). An increase MAPKp42/44 occurred only after rilmenidine. Furthermore, pretreatment efaroxan (0.15 μg/rat i.c.), antagonist, PD98059 (2′-amino-3′-methoxyflavone) (5 extracellular signal-regulated 1/2 inhibitor, significantly attenuated i.c. The findings suggest induced presents vivo distinguishes neuronal triggered from those α2-adrenergic receptor.