Ferreira Hilda Silva, de Castro e Silva Emilio, Cointeiro Carla, Oliveira Elenilda, Faustino Thiallan Nery, Fregoneze Josmara Bartolomei
Life Sciences Department, Bahia State University, 41195-001 Salvador, Bahia, Brazil.
Brain Res. 2004 Nov 26;1028(1):48-58. doi: 10.1016/j.brainres.2004.08.063.
The aim of the present study was to investigate the participation of central 5-HT(3) receptors in the control of blood pressure and heart rate (HR) of non-stressed and stressed rats. The pharmacological stimulation of brain 5-HT(3) receptors by third ventricle injections of the selective 5-HT(3) receptor agonist m-CPBG induced a significant decrease in blood pressure in non-stressed rats and impaired the hypertensive response induced by restraint stress. The blockade of brain 5-HT(3) receptors by the central administration of the selective 5-HT(3) antagonist ondansetron elicited a significant increase in blood pressure in non-stressed rats. Conversely, the hypertensive response induced by restraint stress was not affected by central administration of ondansetron. Additionally, baroreflex-mediated bradycardia during phenylephrine-induced hypertensive response was preserved in non-stressed animals receiving third ventricle injections of m-CPBG, while the baroreflex-mediated tachycardia that occurs during the hypotensive response induced by the administration of sodium nitroprusside was impaired. It is concluded that the serotoninergic component represented by the brain 5-HT(3) receptors exerts a tonic inhibitory influence on the central control of blood pressure in non-stressed rats, probably by a sympathoinhibitory-related mechanism. On the other hand, during stress, this central 5-HT(3)-dependent inhibitory drive is overwhelmed by the different neurochemical systems that harmonically trigger and sustain the hypertensive response.
本研究的目的是探讨中枢5-羟色胺(5-HT)3受体在非应激和应激大鼠血压及心率(HR)调控中的作用。通过向第三脑室注射选择性5-HT3受体激动剂间氯苯甲酰胺(m-CPBG)对脑5-HT3受体进行药理学刺激,可使非应激大鼠血压显著降低,并削弱束缚应激诱导的高血压反应。通过向中枢给予选择性5-HT3拮抗剂昂丹司琼阻断脑5-HT3受体,可使非应激大鼠血压显著升高。相反,束缚应激诱导的高血压反应不受中枢给予昂丹司琼的影响。此外,在接受第三脑室注射m-CPBG的非应激动物中,去氧肾上腺素诱导的高血压反应期间压力反射介导的心动过缓得以保留,而硝普钠给药诱导的低血压反应期间发生的压力反射介导的心动过速则受到损害。结论是,脑5-HT3受体所代表的5-羟色胺能成分对非应激大鼠的血压中枢调控具有紧张性抑制作用,可能是通过与交感神经抑制相关的机制实现的。另一方面,在应激期间,这种中枢5-HT3依赖性抑制驱动被协调触发和维持高血压反应的不同神经化学系统所压倒。