Wang H, Lu Z, Yuan W
Department of Cardiology, First Affiliated Hospital of Xi'an Medical University, China.
Chin Med J (Engl). 1997 Dec;110(12):911-4.
To compare the effect of ouabain on the blood pressure of rats with that of digoxin to find the evidences of the relationship between endogenous ouabain (EO) and development of hypertension.
Sprague-Dawley rats, which were divided into 3 groups, were infused with ouabain (23 x 75 micrograms.kg-1/day, i.p.), digoxin (36 x 84 micrograms.kg-1/day, i.p.) and normal saline (NS) once a day respectively. Systolic blood pressure and body weight were recorded weekly. Five weeks later, rats of ouabain group were randomly assigned to three infusion subgroups: Oc group, continued with ouabain infusion; Od group, added digoxin (73 x 68 micrograms.kg-1/day, i.p.) and Os group, stopped administration of ouabain. Another week later, direct blood pressure was recorded in aorta. Systolic and diastolic cardiac function, plasma renin activity and aldosterone levels of all the rats were measured.
After a latent period of one week, blood pressure of Ouabain group increased significantly [95.4 +/- 11.8 mmHg (1 mmHg = 0.133 kPa) at the beginning of the experiment vs 122.5 +/- 16.9 mmHg at the end of week 6, P < 0.05] with normal plasma renin activity and higher aldosterone (1.28 +/- 0.45 ng/ml vs 0.69 +/- 0.27 ng/ml, P < 0.05). The blood pressure decreased after either withdrawal of ouabain or addition of digoxin (116.3 +/- 14.4 mmHg vs 100 +/- 10.7 mmHg, P < 0.05; 123.9 +/- 13.9 vs 103.3 +/- 10.5 mmHg, P < 0.05, respectively). No difference of blood pressure was found between the digoxin and NS group.
Our results suggested that EO might be one of the causes of the development of hypertension. Aldosterone might play some role in the mechanism of ouabain-induced hypertension. Digoxin can not induce hypertension. There is a great difference between the effect of ouabain and digoxin on the blood pressure. Moreover, digoxin can reverse the hypertension induced by ouabain.
比较哇巴因与地高辛对大鼠血压的影响,以寻找内源性哇巴因(EO)与高血压发生之间关系的证据。
将Sprague-Dawley大鼠分为3组,分别每天腹腔注射一次哇巴因(23×75微克·千克⁻¹/天)、地高辛(36×84微克·千克⁻¹/天)和生理盐水(NS)。每周记录收缩压和体重。5周后,将哇巴因组大鼠随机分为3个注射亚组:Oc组,继续注射哇巴因;Od组,加用地高辛(73×68微克·千克⁻¹/天,腹腔注射);Os组,停止注射哇巴因。再过1周后,记录主动脉直接血压。测定所有大鼠的收缩和舒张心功能、血浆肾素活性及醛固酮水平。
经过1周的潜伏期后,哇巴因组血压显著升高[实验开始时为95.4±11.8 mmHg(1 mmHg = 0.133 kPa),第6周结束时为122.5±16.9 mmHg,P < 0.05],血浆肾素活性正常,醛固酮水平升高(1.28±0.45纳克/毫升对0.69±0.27纳克/毫升,P < 0.05)。停用哇巴因或加用地高辛后血压均下降(分别为116.3±14.4 mmHg对100±10.7 mmHg,P < 0.05;123.9±13.9对103.3±10.5 mmHg,P < 0.05)。地高辛组与生理盐水组血压无差异。
我们的结果提示,EO可能是高血压发生的原因之一。醛固酮可能在哇巴因诱导的高血压机制中起一定作用。地高辛不会诱发高血压。哇巴因与地高辛对血压的影响有很大差异。此外,地高辛可逆转哇巴因诱导的高血压。