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①在麻醉、自然呼吸的家兔上观察到,第四脑室注射促甲状腺素释放激素(TRH)5μg,动脉血压(BP)升高3.2±0.6kPa,,心率(HR)减慢。第四脑室预注射哌唑嗪(1μg),使TRH的升压效应减弱52.1±0.6％。②在麻醉、制动及人工呼吸的家兔上观察到,第四脑室注射TRH(5μg),肾神经放电(PND)频率和BP分别增高185.0±46.3％和36.6±6.5％。静脉预注射哌唑嗪(2mg)或心得安(2mg)对TRH的RND频率增加效应无明显影响,但均使TRH的升高血压效应明显减弱。结果表明,TRH具有中枢升压作用,此作用部分是由脑内α_1受体介导。其外周机理主要是通过兴奋交感神经,使外周血管收缩,并通过激活肾近球细胞的β受体,促进肾素释放,导致血压升高。
① In anesthetized and spontaneous rabbits, 5 μg of TRH was injected into the fourth ventricle. The arterial blood pressure (BP) increased 3.2 ± 0.6 kPa and the heart rate (HR) slowed down. In the fourth ventricle, prazosin (1 μg) was pre-injected, reducing the voltage increasing effect of TRH by 52.1 ± 0.6%. ② In rabbits anesthetized, braked and resuscitated, the fourth ventricle injection of TRH (5 μg) and PND increased by 185.0 ± 46.3% and 36.6 ± 6.5%, respectively. Intravenous pre-injection of prazosin (2mg) or propranolol (2mg) had no effect on the increase of RND frequency in TRH, but both significantly reduced the effect of elevated blood pressure of TRH. The results showed that TRH has central vasopressors, and this effect is partly mediated by the alpha 1 receptors in the brain. The peripheral mechanism is mainly through the excitement of the sympathetic nerve, the peripheral vasoconstriction, and by activating the proximal receptor of renal proximal beta cells, promote renin release, resulting in elevated blood pressure.