Browning R A, Bramlet D G, Myers J H, Bundman M C, Smith M L
Clin Exp Hypertens (1978). 1981;3(5):953-73. doi: 10.3109/10641968109033715.
Spontaneously hypertensive (SH) and normotensive (Wistar-Kyoto, WKY) rats were examined for blood pressure changes following depletion of CNS serotonin (5-HT) by 3 separate techniques: (1) p-chlorophenylalanine, (2) 5,7-dihydroxytryptamine, and (3) a lesion of the dorsal and median raphe nuclei. All of these procedures failed to alter blood pressure in either hypertensive or normotensive rats, despite marked reductions (75-85%) in forebrain 5-HT. Moreover, treatment of 10 day-old hypertensive rat pups with intracisternal injections of 5,7-DHT (10 microgram) failed to alter the development of hypertension despite a 75-80% decrease in spinal cord 5-HT. These findings, which show that 5-HT depletion does not alter blood pressure in the SH or the WKY rat, do not lend support to the idea that 5-HT is involved in the regulation of blood pressure or in the development and maintenance of hypertension in the SH rat.
通过三种不同技术耗尽中枢神经系统5-羟色胺（5-HT）后，对自发性高血压（SH）大鼠和正常血压（Wistar-Kyoto，WKY）大鼠的血压变化进行了检测：（1）对氯苯丙氨酸，（2）5,7-二羟基色胺，以及（3）损毁背侧和中缝核。尽管前脑5-HT显著降低（75-85%），但所有这些操作均未能改变高血压大鼠或正常血压大鼠的血压。此外，对10日龄的高血压大鼠幼崽进行脑池内注射5,7-DHT（10微克）治疗，尽管脊髓5-HT减少了75-80%，但未能改变高血压的发展。这些结果表明，5-HT耗竭不会改变SH大鼠或WKY大鼠的血压，不支持5-HT参与血压调节或SH大鼠高血压的发生和维持这一观点。
