Takahashi H, Buñag R D
J Pharmacol Exp Ther. 1981 Jan;216(1):192-7.
Central actions of bradykinin were studied by recording blood pressure and sympathetic nerve activity from the body of a recipient rat whose head was vascularly isolated and perfused by a donor rat. Intracarotid injections of bradykinin had biphasic effects consisting of initial inhibition followed by more prolonged stimulation. Initial vasodepression and sympathetic inhibition disappeared after intracerebroventricular injection of 6-hydroxydopamine. On the other hand, the secondary pressor response and its attendant sympathetic hyperactivity were reduced after inhibition of prostaglandin synthesis with indomethacin, and conversely, augmented after administration of the prostaglandin precursor, arachidonic acid. Pressor responses elicited by intracerebroventricular injection of bradykinin in awake rats were also inhibited by indomethacin. These results indicate that bradykinin has at least two centrally induced actions on blood pressure: an initial vasodepression caused by release of endogenous norepinephrine which activates alpha adrenergic vasodepressor mechanisms in supramedullary centers, and a secondary pressor effect that may be mediated via release of endogenous prostaglandins.
通过记录头部经血管分离并由供体大鼠灌注的受体大鼠身体的血压和交感神经活动，研究了缓激肽的中枢作用。颈内注射缓激肽产生双相效应，包括最初的抑制作用，随后是更持久的刺激作用。脑室内注射6-羟基多巴胺后，最初的血管舒张和交感神经抑制消失。另一方面，用吲哚美辛抑制前列腺素合成后，继发性升压反应及其伴随的交感神经活动亢进减弱，相反，给予前列腺素前体花生四烯酸后则增强。吲哚美辛也抑制清醒大鼠脑室内注射缓激肽引起的升压反应。这些结果表明，缓激肽对血压至少有两种中枢诱导作用：一种是由内源性去甲肾上腺素释放引起的最初血管舒张，内源性去甲肾上腺素激活髓上中枢的α肾上腺素能血管舒张机制；另一种是继发性升压效应，可能通过内源性前列腺素的释放介导。
