首页> 外文期刊>Journal of applied physiology >Involvement of central angiotensin II type 1 receptors in LPS-induced systemic vasopressin release and blood pressure regulation in rats.
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Involvement of central angiotensin II type 1 receptors in LPS-induced systemic vasopressin release and blood pressure regulation in rats.

机译:中央血管紧张素II 1型受体参与LPS诱导的大鼠系统性加压素释放和血压调节。

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The purpose of this study was to evaluate the involvement of central angiotensin II (ANG II) and ANG II type 1 (AT(1)) receptors in systemic release of arginine vasopressin (AVP) and blood pressure regulation during endotoxemia. LPS (150 microg/kg) was injected intravenously 30 min after intracerebroventricular (icv) losartan (50 microg), an AT(1) receptor antagonist, or subcutaneous (sc) captopril (50 mg/kg), an angiotensin-converting enzyme inhibitor. Rats with icv and sc saline injections served as control. LPS administration increased plasma AVP concentration from 2.1 +/- 0.2 to 15.2 +/- 2.5 pg/ml (60 min after LPS injection) without significant changes in plasma osmolality or hematocrit. LPS-induced AVP secretion was significantly attenuated by pretreatment with icv losartan (2.3 +/- 0.5 to 3.7 +/- 0.5 pg/ml) but was not attenuated after peripheral captopril treatment (2.2 +/- 0.6 to 17.6 +/- 4.2 pg/ml). LPS administration significantly decreased systolic blood pressure (SBP) by 22.7 +/- 5.4 mmHg after intravenous LPS injection in icv losartan-treated rats, while SBP remained unchanged in vehicle-treated or sc captopril-treated rats by intravenous LPS. These results indicate that central AT(1) receptors, not responsive to peripheral ANG II, play an important role in systemic AVP secretion and maintenance of blood pressure during endotoxemia.
机译:这项研究的目的是评估中枢血管紧张素II(ANG II)和ANG II 1型(AT(1))受体在内毒素血症期间全身释放精氨酸加压素(AVP)和血压调节中的作用。在脑室内(icv)氯沙坦(50 microg),一种AT(1)受体拮抗剂或皮下(sc)卡托普利(50 mg / kg),一种血管紧张素转换酶抑制剂后30分钟静脉注射LPS(150 microg / kg) 。注射icv和sc盐水的大鼠作为对照。施用LPS可使血浆AVP浓度从2.1 +/- 0.2 pg / ml增至15.2 +/- 2.5 pg / ml(LPS注射后60分钟),血浆渗透压或血细胞比容无明显变化。 LPS诱导的AVP分泌通过用icv氯沙坦预处理(2.3 +/- 0.5至3.7 +/- 0.5 pg / ml)显着减弱,但在外周卡托普利治疗后未减弱(2.2 +/- 0.6至17.6 +/- 4.2 pg) / ml)。在接受icv氯沙坦治疗的大鼠中,静脉内LPS注射后,给予LPS可使收缩压(SBP)显着降低22.7 +/- 5.4 mmHg,而通过静脉内LPS的媒介物治疗或卡托普利治疗的大鼠中,SBP保持不变。这些结果表明,中央AT(1)受体,对外周ANG II不响应,在内毒素血症期间在全身AVP分泌和血压维持中起重要作用。

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