Ni H, Zhang X H
Department of Physiology, Nanjing Medical College.
Sheng Li Xue Bao. 1993 Apr;45(2):149-57.
In the present investigation changes of pulmonary and carotid arterial pressure in response to injection of substance P(SP) into the 4th ventricle of rabbits were studied. The results were as follows: (1) Intraventricular (ivt.) injection of SP could induce either an increase or a decrease in pulmonary arterial pressure as well as carotid arterial pressor response and bradycardia. (2) Bilateral cervical vagotomy could initiate a definite pulmonary pressor response and a marked decrease in the bradycardiac response to injection of SP in those rabbits originally showing a depressor response of pulmonary artery to SP. (3) Pretreatment by i.c.v. and i.v. phentolamine or alpha 1 blocker, prazosin, could block both the SP-induced pulmonary and carotid pressor responses. (4) alpha 2 blocker, yohimbine, or naloxone could enhance the pressor responses in the both arteries. (5) Propranolol had no effect on the pressor responses in both arteries. (6) The cardiovascular responses to SP could be blocked by the SP blocker (D-Pro2.D-Trp7.9)-SP. It is assumed that increase of SP in the brain may induce an increase in both the pulmonary and carotid arterial pressures and bradycardia by activating the SP receptors. The central mechanism responsible for the SP- induced pressor response involves the participation of adrenergic alpha 1 receptor activities, while the central adrenergic alpha 2 receptor system as well as the endorphin system exerts an inhibitory modulation on the central SP-induced pressor pathway. It appears that SP, catecholamine and opiate substance are all involved in the regulation of blood pressure by brain stem.
在本研究中,观察了向家兔第四脑室内注射P物质(SP)后肺和颈动脉血压的变化。结果如下:(1)脑室内注射SP可引起肺动脉压升高或降低,以及颈动脉升压反应和心动过缓。(2)双侧颈迷走神经切断可在原本对SP呈现肺动脉降压反应的家兔中引发明确的肺升压反应,并使注射SP后的心动过缓反应明显减弱。(3)脑室内和静脉注射酚妥拉明或α1受体阻滞剂哌唑嗪预处理可阻断SP诱导的肺和颈动脉升压反应。(4)α2受体阻滞剂育亨宾或纳洛酮可增强两条动脉的升压反应。(5)普萘洛尔对两条动脉的升压反应无影响。(6)SP受体阻滞剂(D-Pro2.D-Trp7.9)-SP可阻断对SP的心血管反应。推测脑内SP增加可能通过激活SP受体导致肺动脉和颈动脉压升高及心动过缓。SP诱导的升压反应的中枢机制涉及肾上腺素能α1受体活性的参与,而中枢肾上腺素能α2受体系统以及内啡肽系统对中枢SP诱导的升压途径发挥抑制性调节作用。看来SP、儿茶酚胺和阿片类物质均参与脑干对血压的调节。