Majima M, Adachi K, Kuribayashi Y, Mizogami S, Katori M
Department of Pharmacology, Kitasato University School of Medicine, Kanagawa, Japan.
Jpn J Pharmacol. 1995 Oct;69(2):149-58. doi: 10.1254/jjp.69.149.
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. Intraarterial (i.a.) infusion (6 ml/kg/hr) of conscious deficient BN-Ka rats with 0.15 M NaCl 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 NaCl 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 NaCl 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 NaCl-infused deficient BN-Ka rats shifted to the left by a factor of 10 compared with that in 0.15 M NaCl-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 NaCl. 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.
与同一品系的正常棕色挪威北里（正常BN-Ki）大鼠相比，激肽原缺乏的棕色挪威天主教大鼠（缺陷型BN-Ka）尿中排出少量激肽。对清醒的缺陷型BN-Ka大鼠进行动脉内（i.a.）输注（6 ml/kg/小时）0.15 M NaCl，平均动脉血压（MBP）未升高[从103±2（术前）升至93±6 mmHg（第4天）]，血清、脑脊液或红细胞中也未出现钠蓄积，但输注0.3 M NaCl可使MBP从104±3（术前）显著升至130±5 mmHg（第4天），同时血清、脑脊液和红细胞中的钠水平升高。在正常BN-Ki大鼠中输注0.3 M NaCl，MBP既未升高，钠也未蓄积。与输注0.15 M NaCl的缺陷型BN-Ka大鼠相比，在输注0.3 M NaCl的缺陷型BN-Ka大鼠中，血管紧张素II注射（i.a.，推注，1-1000 pmol/kg）导致MBP升高的剂量反应曲线向左移动了10倍，去甲肾上腺素注射导致的曲线向左移动了30倍。正常BN-Ki大鼠在输注0.3 M NaCl时，MBP升高未表现出任何增强。这些结果表明，由于激肽生成缺乏导致的钠蓄积可能与血管对血管紧张素II和去甲肾上腺素的反应性增加有关。
