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首页> 外文期刊>American Journal of Physiology >Role of bradykinin B1 and B2 receptors in normal blood pressure regulation.
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Role of bradykinin B1 and B2 receptors in normal blood pressure regulation.

机译：缓激肽B1和B2受体在正常血压调节中的作用。

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With inhibition or absence of the bradykinin B2 receptor (B2R), B1R is upregulated and assumes some of the hemodynamic properties of B2R, indicating that both participate in the maintenance of normal vasoregulation or to development of hypertension. Herein we further evaluate the role of bradykinin in normal blood pressure (BP) regulation and its relationship with other vasoactive factors by selectively blocking its receptors. Six groups of Wistar rats were treated for 3 wk: one control group with vehicle alone, one with concurrent administration of B1R antagonist R-954 (70 microg x kg(-1) x day(-1)) and B2R antagonist HOE-140 (500 microg x kg(-1) x day(-1)), one with R-954 alone, one with HOE 140 alone, one with concurrent administration of both R-954 and HOE-140 plus the angiotensin antagonist losartan (5 mg x kg(-1) x day(-1)), and one with only losartan. BP was measured continuously by radiotelemetry. Only combined administration of B1R and B2R antagonists produced a significant BP increase from a baseline of 107-119 mmHg at end point, which could be partly prevented by losartan and was not associated with change in catecholamines, suggesting no involvement of the sympathoadrenal system. The impact of blockade of bradykinin on other vasoregulating systems was assessed by evaluating gene expression of different vasoactive factors. There was upregulation of the eNOS, AT1 receptor, PGE2 receptor, and tissue kallikrein genes in cardiac and renal tissues, more pronounced when both bradykinin receptors were blocked; significant downregulation of AT2 receptor gene in renal tissues only; and no consistent changes in B1R and B2R genes in either tissue. The results indicate that both B1R and B2R contribute to the maintenance of normal BP, but one can compensate for inhibition of the other, and the chronic inhibition of both leads to significant upregulation in the genes of related vasoactive systems.
机译：在缓激肽B2受体（B2R）受抑制或不存在的情况下，B1R被上调并呈现B2R的某些血液动力学特性，表明两者均参与维持正常的血管舒张或高血压的发展。在本文中，我们通过选择性阻断其受体来评估缓激肽在正常血压（BP）调节中的作用及其与其他血管活性因子的关系。六组Wistar大鼠进行了3周的治疗：一个对照组单独使用媒介物，一组同时施用B1R拮抗剂R-954（70 microg x kg（-1）x day（-1））和B2R拮抗剂HOE-140 （500 microg x kg（-1）x day（-1）），一种单独使用R-954，一种单独使用HOE 140，一种同时使用R-954和HOE-140以及血管紧张素拮抗剂洛沙坦（5 mg x kg（-1）x day（-1）），仅含氯沙坦。通过无线电遥测法连续测量BP。仅B1R和B2R拮抗剂的联合给药在终点时使基线血压从107-119 mmHg的基线显着升高，这可以部分由氯沙坦预防，并且与儿茶酚胺的变化无关，这表明交感肾上腺系统不参与。通过评估不同血管活性因子的基因表达，评估缓激肽对其他血管调节系统的影响。心脏和肾脏组织中的eNOS，AT1受体，PGE2受体和组织激肽释放酶基因上调，而这两种缓激肽受体均被阻滞则更为明显。仅在肾组织中显着下调AT2受体基因;而且两种组织中的B1R和B2R基因均无一致变化。结果表明，B1R和B2R都有助于维持正常的BP，但是一个可以补偿另一个对BP的抑制作用，并且两者的长期抑制导致相关血管活性系统基因的显着上调。

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