Campbell W B, Schmitz J M, Itskovitz H D
Endocrinology. 1977 Jan;100(1):46-51. doi: 10.1210/endo-100-1-46.
The steroidogenic and pressor activities of the nonapeptide (des-Asp1) angiotensin I [(des-Asp)-AI] were tested in conscious rats. (des-Asp)-AI caused dose related increases in mean arterial pressure (MAP), serum aldosterone, and serum corticosterone in doses between 3 and 3,000 ng/kg/min. (des-Asp)-AI was 14% as potent as angiotensin I and angiotensin II and 60% as potent as (des-Asp1) angiotensin II [des-Asp)-AII] in raising MAP. (des-Asp)-AI was less active than AI, AII, or (des-Asp)-AII in causing increased release of aldosterone, possessing only 8%, 11%, and 17% of the potency of AII, (des-Asp)-AII, and AI, respectively. Each of these angiotensin peptides was equally potent in elevating serum corticosterone levels. Infusions of a nonapeptide inhibitor of converting enzyme (CEI, 0.5 mg/kg/min iv) did not alter control MAP or blood pressure responses to AII or (des-Asp-)-AII but inhibited equally the blood pressure effects of AI and (des-Asp)-AI. CEI also inhibited the ability of (des-Asp)-AI (67% inhibition) and AI (34% inhibition) to increase the serum aldosterone concentration, but had no effect on basal aldosterone levels. These data indicate that (des-Asp)-AI has pressor and steroidogenic effects, but requires conversion to (des-Asp)-AII for a major portion of its activity. These results further substantiate the hypothesis that (des-Asp)-AII, recently recognized as a hormone of the renin-angiotensin system, may be produced without the formation of AII as an intermediate and provide in vivo evidence for the conversion of (des-Asp)-AI to (des-Asp)-AII.
在清醒大鼠中测试了九肽（去天冬氨酸1）血管紧张素I [（去天冬氨酸）-AI]的类固醇生成活性和升压活性。（去天冬氨酸）-AI在3至3000 ng/kg/min的剂量范围内可引起平均动脉压（MAP）、血清醛固酮和血清皮质酮剂量相关的升高。在升高MAP方面，（去天冬氨酸）-AI的效力是血管紧张素I和血管紧张素II的14%，是（去天冬氨酸1）血管紧张素II [（去天冬氨酸）-AII]的60%。在引起醛固酮释放增加方面，（去天冬氨酸）-AI的活性低于AI、AII或（去天冬氨酸）-AII，其效力分别仅为AII、（去天冬氨酸）-AII和AI的8%、11%和17%。这些血管紧张素肽在升高血清皮质酮水平方面的效力相同。输注一种转化酶的九肽抑制剂（CEI，0.5 mg/kg/min静脉注射）不会改变对照MAP或对AII或（去天冬氨酸）-AII的血压反应，但同样抑制AI和（去天冬氨酸）-AI的血压效应。CEI还抑制（去天冬氨酸）-AI（67%抑制）和AI（34%抑制）增加血清醛固酮浓度的能力，但对基础醛固酮水平无影响。这些数据表明，（去天冬氨酸）-AI具有升压和类固醇生成作用，但其大部分活性需要转化为（去天冬氨酸）-AII。这些结果进一步证实了以下假设，即最近被认为是肾素-血管紧张素系统一种激素的（去天冬氨酸）-AII可能在不形成AII作为中间产物的情况下产生，并为（去天冬氨酸）-AI转化为（去天冬氨酸）-AII提供了体内证据。
