Tsuda K, Nishio I, Masuyama Y
Department of Medicine, Wakayama Medical College, Japan.
Clin Exp Hypertens A. 1987;9(10):1601-14. doi: 10.3109/10641968709159005.
This study was performed to investigate prostaglandin (PG)-mediated regulation of norepinephrine release from the sympathetic nerve endings in spontaneously hypertensive rats (SHR). The effects of PGE2 on the pressor responses and norepinephrine overflow during the periarterial nerve stimulation were examined in the perfused mesenteric vascular beds from SHR and age-matched Wistar Kyoto rats (WKY). In preliminary studies using normotensive Wistar rats, PGE2 inhibited the overflow of norepinephrine in response to the electrical nerve stimulation. On the contrary, when indomethacin was infused into the preparations, the norepinephrine overflow induced by the nerve stimulation was increased. In SHR, the neurogenic vasoconstriction and norepinephrine overflow during the nerve stimulation were significantly greater than in WKY. PGE2 in the medium inhibited the pressor responses and norepinephrine overflow during the nerve stimulation dose-dependently in WKY, while the inhibitory effects of PGE2 in SHR were blunted. These results suggest that PGE2 is an important hormone in regulating sympathetic vascular tone and that presynaptic inhibition of vascular adrenergic transmission by PGE2 is attenuated in SHR.
本研究旨在探讨前列腺素(PG)介导的自发性高血压大鼠(SHR)交感神经末梢去甲肾上腺素释放的调节机制。在SHR和年龄匹配的Wistar Kyoto大鼠(WKY)的灌注肠系膜血管床中,检测了PGE2对动脉周围神经刺激期间升压反应和去甲肾上腺素溢出的影响。在使用正常血压Wistar大鼠的初步研究中,PGE2抑制了电神经刺激引起的去甲肾上腺素溢出。相反,当将吲哚美辛注入制剂中时,神经刺激诱导的去甲肾上腺素溢出增加。在SHR中,神经刺激期间的神经源性血管收缩和去甲肾上腺素溢出明显大于WKY。培养基中的PGE2在WKY中剂量依赖性地抑制神经刺激期间的升压反应和去甲肾上腺素溢出,而PGE2在SHR中的抑制作用减弱。这些结果表明,PGE2是调节交感神经血管张力的重要激素,并且SHR中PGE2对血管肾上腺素能传递的突触前抑制作用减弱。