Hypertension induced by a nonpressor dose of angiotensin II in kininogen-deficient rats.
Hypertension induced by a nonpressor dose of angiotensin II in kininogen-deficient rats.
复制标题
在激肽原缺乏的大鼠中由非升压剂量的血管紧张素 II 诱导的高血压。
作者：
M. Majima;S. Mizogami;Y. Kuribayashi;M. Katori;S. Oh‐ishi
血浆激肽原水平极低的棕色挪威Katholiek大鼠在尿液中排出的激肽量比同品系的正常大鼠少得多。7周龄激肽原缺乏大鼠的收缩压（132 ± 2 mmHg，n = 7）与正常大鼠无差异。血管紧张素II（Ang II）（20微克/天SC）从7周龄开始用微渗透泵给药2周，引起缺陷大鼠血压显著升高（181 +/- 5 mm Hg，n = 7，9周龄），尽管相同的治疗在正常大鼠中没有引起血压升高。此外，在此期间，缺乏大鼠有显着更高的心率，倾向于排泄更少的尿钠，并表现出显着更高的钠水平，血清，红细胞和脑脊液相比，正常大鼠。Ang Ⅱ可增加正常和缺乏大鼠尿醛固酮排泄量（P <0.05）。对缺陷大鼠进行螺内酯治疗（50 mg/kg/天）7天，使血压和心率恢复至正常水平，并显着降低红细胞和脑脊液中的钠水平。皮下输注牛低分子量激肽原与渗透泵在血管紧张素II治疗缺陷大鼠诱导血压，心率和红细胞钠水平显着降低。相比之下，皮下输注缓激肽拮抗剂Hoe 140在血管紧张素II治疗的正常大鼠诱导的高血压反应与心率和红细胞钠水平显着增加平行。这些结果表明，在激肽原缺乏大鼠中观察到的激肽生成的缺乏可能会导致高血压反应，在管理过程中的非升压剂量的血管紧张素II主要通过钠潴留可能引起的醛固酮释放。
Brown Norway Katholiek rats with very low levels of plasma kininogens excreted a much smaller amount of kinin in the urine than normal rats of the same strain. The systolic blood pressure of 7-week-old kininogen-deficient rats (132 +/- 2 mmHg, n = 7) was not different from that of normal rats. Angiotensin II (Ang II) (20 micrograms/d SC) from 7 weeks of age for 2 weeks with a micro-osmotic pump caused significant increases in blood pressure (181 +/- 5 mm Hg, n = 7, 9 weeks old) in the deficient rats, although the same treatment induced no blood pressure increase in the normal rats. Also during this period, the deficient rats had significantly higher heart rates, tended to excrete less urinary sodium, and showed significantly higher sodium levels in serum, erythrocytes, and cerebrospinal fluid compared with the normal rats. Ang II increased urinary excretion of aldosterone in both deficient and normal rats (P < .05). Spironolactone treatment (50 mg/kg per day) for 7 days in deficient rats restored blood pressure and heart rate to normal levels and significantly reduced sodium levels in erythrocytes and cerebrospinal fluid. Subcutaneous infusion of bovine low-molecular-weight kininogen with an osmotic pump in Ang II-treated deficient rats induced significant reductions in blood pressure, heart rate, and erythrocyte sodium levels. By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 in Ang II-treated normal rats induced a hypertensive response in parallel with significant increases in heart rate and erythrocyte sodium level. These results suggest that the lack of kinin generation observed in the kininogen-deficient rats may cause the hypertensive response during the administration of a nonpressor dose of Ang II mainly through sodium retention probably caused by aldosterone release.
影响因子：
8.3
作者：
JOHNSON, RJ;ALPERS, CE;SCHWARTZ, SM
通讯作者：
SCHWARTZ, SM