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首页> 外文期刊>Japanese Journal of Pharmacology >Increase in Vascular Sensitivity to Angiotensin II and Norepinephrine after Four-Day Infusion of 0.3 M Sodium Chloride in Conscious Kininogen-Deficient Brown Norway Katholiek Rats
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Increase in Vascular Sensitivity to Angiotensin II and Norepinephrine after Four-Day Infusion of 0.3 M Sodium Chloride in Conscious Kininogen-Deficient Brown Norway Katholiek Rats

机译：四天输注清醒的缺乏激肽原的褐挪威Katholiek大鼠0.3 M氯化钠后，对血管紧张素II和去甲肾上腺素的血管敏感性增加

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References(26) Cited-By(10) Kininogen-deficient Brown Norway Katholiek (deficient BN-Ka) rats excreted a small amount of kinin in their urine, compared with normal BN Kitasato (normal BN-Ki) rats from the same strain. Intra-arterial (i.a.) infusion (6 ml/kg/hr) of conscious deficient BN-Ka rats with 0.15 M NaCI did not increase mean arterial blood pressure (MBP) [from 103 ± 2 (pre) to 93 ± 6 mmHg (day 4)] and did not cause sodium accumulation in the serum, cerebrospinal fluid or erythrocytes, but 0.3 M NaCI infusion significantly increased MBP from 104 ± 3 (pre) to 130 ± 5 mmHg (day 4) with increased sodium levels in the serum, cerebrospinal fluid and erythrocytes. Infusion of 0.3 M NaCI in normal BN-Ki rats neither increased MBP nor accumulated sodium. The dose-response curve of the increase in MBP for angiotensin II injection (i.a., bolus, 1-1000 pmol/kg) in 0.3 M NaCI-infused deficient BN-Ka rats shifted to the left by a factor of 10 compared with that in 0.15 M NaCI-infused deficient BN-Ka rats, and that for norepinephrine injection shifted to the left by a factor of 30. Normal BN-Ki rats did not show any enhancement in MBP elevation with 0.3 M NaCI. These results suggest that the sodium accumulation attributable to a lack of kinin generation may be related to increased vascular reactivity to angiotensin II and norepinephrine.
机译：参考文献（26）被引用的By（10）缺乏激肽原的褐挪威Katholiek（BN-Ka缺陷）大鼠与同一菌株的正常BN Kitasato（正常BN-Ki）大鼠相比，尿中排泄了少量激肽。用0.15 M NaCI的有意识缺陷的BN-Ka大鼠的动脉内（ia）输注（6 ml / kg / hr）不会使平均动脉血压（MBP）[从103±2（pre）升高至93±6 mmHg（ [第4天]并没有引起钠在血清，脑脊液或红细胞中的蓄积，但是0.3M NaCl输注可将MBP从104±3（前）显着增加至130±5 mmHg（第4天），并且血清中的钠水平会增加，脑脊液和红细胞。在正常BN-Ki大鼠中输注0.3 M NaCl既不会增加MBP，也不会累积钠。在0.3M输注NaCl的BN-Ka缺乏大鼠中，血管紧张素II注射后MBP的剂量-响应曲线（ia，推注，1-1000 pmol / kg）向左移动了10倍，而与之相比。注入0.15 M NaCl的BN-Ka缺陷大鼠，去甲肾上腺素注射的大鼠向左偏移30倍。正常BN-Ki大鼠在0.3 M NaCl下未显示MBP升高任何增强。这些结果表明归因于缺乏激肽生成的钠积累可能与对血管紧张素II和去甲肾上腺素的血管反应性增加有关。

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