Clonidine prevents enhancement of spinal sympathetic transmission by phosphodiesterase inhibitors.
Preganglionic sympathetic discharges, evoked by cervical stimulation in spinal cats, were rapidly and markedly enhanced for 1-2 h by aminophylline or isobutylmethylxanthine. Clonidine depressed intraspinal transmission and prevented enhancement by the xanthines; alpha 2-receptor antagonists blocked the effect of clonidine and not only restored but also markedly prolonged the enhancement by the xanthines. The results suggest that the excitability of sympathetic preganglionic neurons is regulated by cyclic AMP through activation of different subtypes of adrenergic receptors that are either positively or negatively coupled to adenylate cyclase.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000262:Adenylyl Cyclases / Q000378:metabolism; D000320:Adrenergic Fibers / Q000187:drug effects*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000628:Aminophylline / Q000494:pharmacology; D000818:Animals; D001339:Autonomic Fibers, Preganglionic / Q000187:drug effects*; D002415:Cats; D003000:Clonidine / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D009474:Neurons / Q000187:drug effects; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D009435:Synaptic Transmission / Q000187:drug effects*
D000317:Adrenergic alpha-Antagonists; D010726:Phosphodiesterase Inhibitors; D000628:Aminophylline; D000242:Cyclic AMP; D000262:Adenylyl Cyclases; D003000:Clonidine; D015056:1-Methyl-3-isobutylxanthine