Orer Hakan S, Gebber Gerard L, Barman Susan M
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA.
Am J Physiol Regul Integr Comp Physiol. 2008 May;294(5):R1435-44. doi: 10.1152/ajpregu.00012.2008. Epub 2008 Mar 12.
We studied the changes in inferior cardiac sympathetic nerve discharge (SND) produced by unilateral microinjections of 5-hydroxytryptamine (5-HT) receptor agonists and antagonists into the ventrolateral medulla (VLM) of urethane-anesthetized, baroreceptor-denervated cats. Microinjection of the 5-HT2 receptor antagonist LY-53857 (10 mM) into either the rostral or caudal VLM significantly reduced (P < or = 0.05) the 10-Hz rhythmic component of basal SND without affecting its lower-frequency, aperiodic component. The selective depression of 10-Hz power was accompanied by a statistically significant decrease in mean arterial pressure (MAP). Microinjection of LY-53857 into the VLM also attenuated the increase in 10-Hz power that followed tetanic stimulation of depressor sites in the caudal medullary raphé nuclei. Microinjection of the 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-amino-propane (DOI; 10 microM) into the VLM selectively enhanced 10-Hz SND, and intravenous DOI (1 mg/kg) partially reversed the reduction in 10-Hz SND produced by 5-HT2 receptor blockade in the VLM. Microinjection of the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OHDPAT; 10 mM), into either the rostral or caudal VLM also selectively attenuated 10-Hz SND and significantly reduced MAP. The reduction in 10-Hz SND produced by 8-OHDPAT was partially reversed by intravenous WAY-100635 (1 mg/kg), which selectively blocks 5-HT1A receptors. These results support the view that serotonergic inputs to the VLM play an important role in expression of the 10-Hz rhythm in SND.
我们研究了在氨基甲酸乙酯麻醉、压力感受器去神经支配的猫的腹外侧延髓（VLM）中单侧微量注射5-羟色胺（5-HT）受体激动剂和拮抗剂所产生的心脏下交感神经放电（SND）的变化。向延髓头端或尾端VLM微量注射5-HT2受体拮抗剂LY-53857（10 mM）可显著降低（P≤0.05）基础SND的10 Hz节律成分，而不影响其低频、非周期性成分。10 Hz功率的选择性降低伴随着平均动脉压（MAP）的统计学显著下降。向VLM微量注射LY-53857也减弱了对延髓尾端中缝核减压部位进行强直刺激后10 Hz功率的增加。向VLM微量注射5-HT2受体激动剂1-（2,5-二甲氧基-4-碘苯基）-2-氨基丙烷（DOI；10 μM）可选择性增强10 Hz SND，静脉注射DOI（1 mg/kg）可部分逆转VLM中5-HT2受体阻断所导致的10 Hz SND的降低。向延髓头端或尾端VLM微量注射5-HT1A受体激动剂8-羟基-2-（二正丙基氨基）四氢萘（8-OHDPAT；10 mM）也可选择性减弱10 Hz SND并显著降低MAP。静脉注射选择性阻断5-HT1A受体的WAY-100635（1 mg/kg）可部分逆转8-OHDPAT所导致的10 Hz SND的降低。这些结果支持这样一种观点，即向VLM的5-羟色胺能输入在SND的10 Hz节律表达中起重要作用。
