Trolliet M R, Kurnjek M L, Mikulic L, Basso N, Taquini A C
Instituto de Investigaciones Cardiológicas, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Hypertension. 1990 Feb;15(2 Suppl):I166-9. doi: 10.1161/01.hyp.15.2_suppl.i166.
The participation of the central serotonergic system in the development of two-kidney, two clip (2K2C) Goldblatt renovascular hypertension in the rat has been examined. Half of the rats were treated with desmethylimipramine intraperitoneally and 5,7-dihydroxytryptamine intracisternally; the other half received only desmethylimipramine and the 5,7-dihydroxytryptamine vehicle. Two days later, a silver clip was placed in both renal arteries in half of the rats of each group. A sham operation was performed in the remaining rats. Blood pressure was recorded during the 5 weeks after treatment. At the end of the experiment, blood and cerebrospinal fluid samples were obtained. The brain was dissected into several areas and kept frozen. Norepinephrine, serotonin, angiotensinogen, and renin-like concentration were evaluated in the brain areas. Plasma renin activity and angiotensinogen concentration in the plasma and cerebrospinal fluid were estimated. In the sham-operated groups, blood pressure was lower in the treated than in the control rats. The curve of blood pressure increase, as well as the final blood pressure, was similar in the treated and control 2K2C rats. Serotonin was significantly depleted by the 5,7-dihydroxytryptamine treatment in all brain areas. Treatment did not induce any changes in central norepinephrine concentration. Plasma renin activity was diminished in the treated sham-operated rats. These data indicate that the central serotonin depletion does not prevent the development of hypertension and confirm the role of the amine in normal blood pressure regulation. On the other hand, the peripheral renin-angiotensin system might participate in the development of high blood pressure in serotonin-depleted animals.
已对大鼠双肾双夹（2K2C）戈德布拉特肾血管性高血压发展过程中中枢5-羟色胺能系统的参与情况进行了研究。一半大鼠腹腔注射去甲丙咪嗪并脑池内注射5,7-二羟基色胺；另一半大鼠仅接受去甲丙咪嗪和5,7-二羟基色胺的溶剂。两天后，每组一半大鼠的双侧肾动脉放置银夹。其余大鼠进行假手术。在治疗后的5周内记录血压。实验结束时，采集血液和脑脊液样本。将大脑解剖成几个区域并冷冻保存。评估脑区中的去甲肾上腺素、5-羟色胺、血管紧张素原和肾素样物质的浓度。估计血浆、脑脊液中的血浆肾素活性和血管紧张素原浓度。在假手术组中，治疗组大鼠的血压低于对照组大鼠。治疗组和对照组2K2C大鼠的血压升高曲线以及最终血压相似。5,7-二羟基色胺处理使所有脑区的5-羟色胺显著减少。治疗未引起中枢去甲肾上腺素浓度的任何变化。治疗后的假手术大鼠血浆肾素活性降低。这些数据表明，中枢5-羟色胺耗竭并不能阻止高血压的发展，并证实了该胺在正常血压调节中的作用。另一方面，外周肾素-血管紧张素系统可能参与了5-羟色胺耗竭动物的高血压发展过程。
