Sinaiko A R
Life Sci. 1983 Dec 5;33(23):2269-75. doi: 10.1016/0024-3205(83)90259-x.
The role of the beta-adrenergic nervous and prostaglandin systems in vasodilator-induced activation of the renin-angiotensin system was studied in conscious rats. The plasma renin activity (PRA) response to intravenous hydralazine (0.25, 0.5 and 1 mg/kg body wt.) was compared to the PRA response following administration of similar doses of hydralazine to rats pretreated with either indomethacin (3 mg/kg body wt. i.v.) or indomethacin and propranolol (1 mg/kg body wt. i.v.). PRA increased significantly above control levels after each of the hydralazine doses. In rats pretreated with indomethacin, PRA did not increase with the 0.25 mg/kg dose of hydralazine; increased significantly with the 0.5 mg/kg dose but remained significantly lower than the PRA response in the absence of indomethacin; and increased with the 1 mg/kg dose to a level not significantly different from PRA in rats receiving only hydralazine. When rats were pretreated with indomethacin and propranolol, PRA did not increase significantly in response to either the 0.25 or 0.5 mg/kg doses of hydralazine. Although a statistically significant increase in PRA was noted with the 1 mg/kg dose of hydralazine, the level of PRA achieved was very low and only 15% of that observed with the other two treatment regimens (i.e., hydralazine alone or indomethacin and hydralazine). These results demonstrate that vasodilator-induced renin release is only partially mediated via the prostaglandin system, that the degree of this control is related to the intensity of vasodilator stimulus and that renin release following administration of hydralazine can be attributed almost entirely to activation of the beta-adrenergic nervous and prostaglandin systems.
在清醒大鼠中研究了β-肾上腺素能神经和前列腺素系统在血管扩张剂诱导的肾素-血管紧张素系统激活中的作用。将静脉注射肼屈嗪(0.25、0.5和1mg/kg体重)后的血浆肾素活性(PRA)反应与给用吲哚美辛(3mg/kg体重,静脉注射)或吲哚美辛和普萘洛尔(1mg/kg体重,静脉注射)预处理的大鼠给予相似剂量肼屈嗪后的PRA反应进行比较。每次给予肼屈嗪剂量后,PRA均显著高于对照水平。在用吲哚美辛预处理的大鼠中,0.25mg/kg剂量的肼屈嗪未使PRA升高;0.5mg/kg剂量使其显著升高,但仍显著低于未用吲哚美辛时的PRA反应;1mg/kg剂量使其升高至与仅接受肼屈嗪的大鼠的PRA无显著差异的水平。当大鼠用吲哚美辛和普萘洛尔预处理时,0.25或0.5mg/kg剂量的肼屈嗪均未使PRA显著升高。虽然1mg/kg剂量的肼屈嗪使PRA有统计学显著升高,但达到的PRA水平非常低,仅为其他两种治疗方案(即单独使用肼屈嗪或吲哚美辛和肼屈嗪)所观察到水平的15%。这些结果表明,血管扩张剂诱导的肾素释放仅部分通过前列腺素系统介导,这种控制程度与血管扩张剂刺激强度有关,并且给予肼屈嗪后的肾素释放几乎完全归因于β-肾上腺素能神经和前列腺素系统的激活。