Basso N, Kurnjek M L, Ruiz P, Taquini A C
Instituto de Investigaciones Cardiologicas, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Clin Exp Hypertens. 1993 Jul;15(4):641-62. doi: 10.3109/10641969309041635.
Some reports have stated that central norepinephrine (NE) depletion inhibited the development of hypertension in the rat. On the other hand, this pharmacological treatment induces changes on the central renin-angiotensin system. The present study was designed to follow the development of 2 kidney-2 clip (2k-2c) renovascular hypertension in rats depleted of central NE and to analyze the central and peripheral renin-angiotensin system. Male Wistar rats (n = 40) were used. Half of the animals was injected, intracisternally, with 6-hydroxydopamine (6-OHDA), the remaining rats only received the vehicle. One week later a silver clip was placed on each renal artery on half of the 6-OHDA treated rats and on half of the vehicle treated animals. A sham operation was performed on the remaining rats. Blood pressure was measured weekly during 7 weeks. Then, blood and cerebrospinal fluid (CSF) samples were obtained. The brain was dissected in several areas. NE and angiotensinogen concentration (AoC) were determined in tissue samples. AoC was evaluated in plasma and CSF; plasma renin activity was also measured. Hypertension development was not prevented by central NE depletion, which was significant in all central areas (p < 0.001). Other significant results showed that renal ischemia and/or NE depletion induced a significant increase in angiotensinogen concentration in the hypothalamus (p < 0.01) and in CSF (p < 0.05). In summary: central NE depletion was not able to modify the development of 2 k - 2 c hypertension. Treatment and renal ischemia induced an increase of central AoC.
一些报告指出，中枢去甲肾上腺素（NE）耗竭可抑制大鼠高血压的发展。另一方面，这种药理学处理会引起中枢肾素-血管紧张素系统的变化。本研究旨在追踪中枢NE耗竭的大鼠2肾2夹（2k-2c）肾血管性高血压的发展，并分析中枢和外周肾素-血管紧张素系统。使用雄性Wistar大鼠（n = 40）。一半动物经脑池内注射6-羟基多巴胺（6-OHDA），其余大鼠仅接受赋形剂。一周后，对一半经6-OHDA处理的大鼠和一半接受赋形剂处理的动物的每条肾动脉放置银夹。对其余大鼠进行假手术。在7周内每周测量血压。然后，采集血液和脑脊液（CSF）样本。将脑部分解为几个区域。测定组织样本中的NE和血管紧张素原浓度（AoC）。评估血浆和CSF中的AoC；还测量血浆肾素活性。中枢NE耗竭并不能阻止高血压的发展，这在所有中枢区域都很显著（p < 0.001）。其他显著结果表明，肾缺血和/或NE耗竭导致下丘脑（p < 0.01）和CSF（p < 0.05）中的血管紧张素原浓度显著增加。总之：中枢NE耗竭无法改变2k - 2c高血压的发展。处理和肾缺血导致中枢AoC增加。
