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去氧皮质酮盐(DOCA)/盐大鼠的中枢儿茶酚胺耗竭、血管加压素与血压

Central catecholamine depletion, vasopressin, and blood pressure in the DOCA/NaCl rat.

作者信息

Okuno T, Winternitz S R, Lindheimer M D, Oparil S

出版信息

Am J Physiol. 1983 Jun;244(6):H807-13. doi: 10.1152/ajpheart.1983.244.6.H807.

DOI:10.1152/ajpheart.1983.244.6.H807
PMID:6407335
Abstract

To determine whether impaired arginine vasopressin (AVP) release occurs when DOCA-NaCl hypertension is prevented following chemical sympathectomy with 6-hydroxydopamine (6-OHDA), male Sprague-Dawley rats treated with intraventricular injections of 6-OHDA (250 micrograms X 2) or Merlis solution received deoxycorticosterone acetate (DOCA) implants (100 mg/kg) and drank 0.5% saline. Systolic blood pressure in the 6-OHDA-treated DOCA/NaCl group (139 +/- 4 mmHg) was lower (P less than 0.001) than in the Merlis-DOCA/NaCl group (183 +/- 7 mmHg). 6-OHDA treatment produced widespread catecholamine depletion throughout the central nervous system, including the supraoptic and paraventricular nuclei, the cells of which are known to produce AVP, but hypothalamic, pituitary, and plasma AVP levels were similar in both experimental groups, the latter values averaging 1.5-2 times those of controls. Both groups of rats suppressed AVP secretion appropriately when water loaded. Such suppression, however, had no effect on blood pressure in the hypertensive animals and, furthermore, administration of the AVP antagonist d(CH2)5Tyr(Me)AVP produced small decrements in mean blood pressure of both groups that were not significantly different from responses seen in control normotensive rats. These data demonstrate that 6-OHDA does not prevent DOCA-NaCl hypertension by decreasing AVP levels and suggest that AVP is not necessary for the maintenance of hypertension in this model.

摘要

为了确定在用6-羟基多巴胺(6-OHDA)进行化学交感神经切除术后预防去氧皮质酮-氯化钠(DOCA-NaCl)性高血压时,是否会出现精氨酸加压素(AVP)释放受损的情况,对雄性Sprague-Dawley大鼠进行脑室内注射6-OHDA(250微克×2)或Merlis溶液处理,然后植入醋酸去氧皮质酮(DOCA,100毫克/千克)并饮用0.5%盐水。6-OHDA处理的DOCA/NaCl组的收缩压(139±4毫米汞柱)低于(P<0.001)Merlis-DOCA/NaCl组(183±7毫米汞柱)。6-OHDA处理导致整个中枢神经系统广泛的儿茶酚胺耗竭,包括视上核和室旁核,已知这些核的细胞会产生AVP,但两个实验组的下丘脑、垂体和血浆AVP水平相似,后者的值平均为对照组的1.5至2倍。两组大鼠在水负荷时均能适当抑制AVP分泌。然而,这种抑制对高血压动物的血压没有影响,此外,给予AVP拮抗剂d(CH2)5Tyr(Me)AVP后,两组的平均血压均有小幅下降,与正常血压对照大鼠的反应无显著差异。这些数据表明,6-OHDA不会通过降低AVP水平来预防DOCA-NaCl性高血压,并提示在该模型中,AVP对维持高血压并非必需。

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