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腹侧第三脑室前部损伤对 Dahl 盐敏感大鼠盐性高血压的影响。

Effect of an anteroventral third ventricle lesion on NaCl hypertension in Dahl salt-sensitive rats.

作者信息

Goto A, Ganguli M, Tobian L, Johnson M A, Iwai J

出版信息

Am J Physiol. 1982 Oct;243(4):H614-8. doi: 10.1152/ajpheart.1982.243.4.H614.

Abstract

An anteroventral third ventricle (AV3V) lesion in the brain prevents several forms of experimental hypertension. The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. After the AV3V lesion Dahl S rats received daily injections of either vasopressin (pitressin tannate, 500 mU/kg) or vehicle during 10 wk of 8% high-NaCl diet. Sham-lesioned rats served as controls. The blood pressure in sham-lesioned rats receiving vehicle was 189 mmHg after 10 wk of high-NaCl diet. Lesioned rats given vehicle showed a significantly smaller increase in blood pressure than sham-lesioned rats (P less than 0.001), the blood pressure averaging 161 mmHg at 10 wk. Lesioned rats given vasopressin also showed a smaller increase in blood pressure than sham-lesioned rats (P less than 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesioned rats given vehicle (P less than 0.025). Vasopressin injections corrected the hypernatremia in lesioned rats. In another experiment the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low-NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P less than 0.025). These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats, the reduction in RPPF, when compared with Dahl R rats, with both strains on a low-NaCl intake.

摘要

大脑前腹侧第三脑室(AV3V)损伤可预防多种形式的实验性高血压。本实验旨在确定AV3V损伤是否能预防Dahl盐敏感(S)大鼠的氯化钠诱导性高血压,以及损伤大鼠中报道的血管加压素释放减弱是否有助于AV3V损伤对高血压的保护作用。在AV3V损伤后,Dahl S大鼠在10周的8%高氯化钠饮食期间每天注射血管加压素(鞣酸加压素,500 mU/kg)或赋形剂。假手术损伤大鼠作为对照。接受赋形剂的假手术损伤大鼠在高氯化钠饮食10周后血压为189 mmHg。给予赋形剂的损伤大鼠血压升高幅度明显小于假手术损伤大鼠(P<0.001),10周时平均血压为161 mmHg。给予血管加压素的损伤大鼠血压升高幅度也小于假手术损伤大鼠(P<0.05),但最终平均血压为176 mmHg,显著高于给予赋形剂的损伤大鼠(P<0.025)。血管加压素注射纠正了损伤大鼠的高钠血症。在另一项实验中,研究了AV3V损伤对Dahl S大鼠肾乳头血浆流量(RPPF)的影响。即使在低氯化钠摄入情况下,Dahl S大鼠的RPPF也低于Dahl盐抵抗(R)大鼠。AV3V损伤使S大鼠的RPPF增加了14%(P<0.025)。这些发现表明,Dahl S大鼠中氯化钠诱导性高血压的充分表达需要AV3V区域的完整性,AV3V损伤减轻Dahl S大鼠中氯化钠诱导性高血压的能力部分与血管加压素释放减弱有关。此外,与Dahl R大鼠相比,在低氯化钠摄入情况下,AV3V损伤部分纠正了Dahl S大鼠的一个特征性表现,即RPPF降低。

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