(Des-Asp1) Angiotensin I: A Study of its Pressor and Steroidogenic Activities in Conscious Rats*

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Abstract
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 3000 ng/kg per 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 per min i.v.) 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. (des-Asp)-AI has pressor and steroidogenic effects, but requires conversion to (des-Asp)-AII for a major portion of its activity. (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.