哇巴因或心房钠尿肽对大鼠动脉平滑肌细胞分泌血管紧张素Ⅱ的影响

Effects of Ouabain or Atrial Natriuretic Peptide on Secreting AngiotensinⅡ in Artery Smooth Muscle Cells

目的探讨哇巴因、心房钠尿肽(ANP)对WKY大鼠和自发性高血压大鼠动脉平滑肌细胞(ASMC)自分泌血管紧张素Ⅱ(AngⅡ)的影响。方法组织块种植法培养4只自发性高血压大鼠和4只WKY大鼠胸主动脉平滑肌细胞,用低、中、高3种浓度(分别为1×10-9mol/L、1×10-8mol/L、1×10-7mol/L)哇巴因、ANP干预两种大鼠ASMC,放射免疫法测定干预前及干预后24 h培养液中AngⅡ水平。1×10-7mol/L哇巴因、ANP干预自发性高血压大鼠和WKY大鼠ASMC,测定干预前及干预后3 h、6 h、12 h、24 h培养液中AngⅡ水平。结果 WKY大鼠AngⅡ水平(8.48±2.50 pg/106cells)低于自发性高血压大鼠(14.06±4.62 pg/106cells),差异无统计学意义。哇巴因干预后,两种大鼠AngⅡ水平显著增加,WKY大鼠在干预12 h达到峰值(36.11±5.34 pg/106cells),自发性高血压大鼠在干预6 h达到峰值(39.31±3.61 pg/106cells);随哇巴因浓度增高,两种大鼠AngⅡ水平呈浓度依赖性升高,在WKY大鼠升高更明显。ANP干预后,两种大鼠AngⅡ水平迅速增加,WKY大鼠在3 h达到峰值(39.75±6.71pg/106cells),自发性高血压大鼠AngⅡ水平随时间延长进行性升高;随ANP浓度增高,WKY大鼠AngⅡ水平升高幅度呈浓度依赖性降低,自发性高血压大鼠AngⅡ水平升高幅度呈浓度依赖性增高。结论哇巴因、ANP明显促进WKY大鼠和自发性高血压大鼠ASMC分泌AngⅡ,哇巴因使自发性高血压大鼠ASMC分泌AngⅡ的高峰前移;ANP促进自发性高血压大鼠ASMC分泌AngⅡ失常。

Aim To investigate the effects of ouabain or atrial natriuretic peptide （ANP） on angiotensin II secreted by artery smooth muscle cells （ASMC） in WKY rats and spontaneously hypertensive rats （SHR）. Methods The thoracic ASMC isolated from SHR and WKY rats were cultured and interfered with different concentrations of ANP or ouabain （ 1 × 10 -9 mol/L, 1 × 10 -8 mol/L and 1 × 10 -7 mol/L） respectively. The levels of angiotensin II in culture-medium were measured by radioimmunoassay before and after 3, 6, 12, and 24 hours of using ouabain or ANP （ 1 × 10 -7 mol/L）. Results Angiotensin II level in WKY rats was lower than that in SHR. After using ouabain, angiotensin ii level of two kinds of rats was remarkably increased, but in WKY rats angiotensin II level reached the peak after 12 hours, while in SHR reached the peak after 6 hours. With the increasing concentration of ouabain, angiotensin II level in WKY rats was increased in a concentration-dependent manner, and in SHR increased in a concentration-independent manner. After using ANP, the level of angiotensin II of two kinds of rats was significantly increased, but in WKY rats reached the peak after 3 hours, and in SHR increased in a time-dependent manner. With the increase of concentration of ANP, the level of angiotensin II went down in WKY rats, whereas went up in SHR. Conclusions Ouabain or ANP can promote the secretion of angiotensin II of ASMC in both WKY rats and SHR, and the secretion peak of angiotensin II induced by ouabain is in advance in SHR. The secretion of Angiotensin II induced by ANP is significantly abnormal in SHR.