Key result
In conscious rats, P-113 inhibited angiotensin II-induced aldosterone release more effectively than angiotensin III-induced release.
Why the study?
Do angiotensin II and angiotensin III induce aldosterone release in conscious rats?
Do angiotensin II and angiotensin III induce aldosterone release in conscious rats?
Angiotensin II and its metabolite angiotensin III both induce aldosterone release in vivo, suggesting angiotensin III may play an important role in this pathway.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications for aldosterone regulation; leaves open species-specific angiotensin pathways for further study.
The potential role of angiotensin II and its heptapeptide metabolite, des-aspartyl-angiotensin II, was studied in the conscious unanesthetized rat. Aldosterone release was induced by both peptides at physiologic doses (0.72 nanogram per minute). [I-Sarcosyl-8-alanyl]-angiotensin II (P-113 inhibited angiotensin II more effectively than des-aspartyl-angiotensin II (101 percent as compared to 82 percent). These results indicate that angiotensin controls aldosterone release in the rat and that des-aspartyl-angiotensin II (that is, angiotensin III) may be important in this sequence.
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Campbell et al. (1974) studied this question. Angiotensin II and Angiotensin III was evaluated on Inhibition of aldosterone release by P-113. In conscious rats, P-113 inhibited angiotensin II-induced aldosterone release more effectively than angiotensin III-induced release.
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