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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Effects of corticotropin-releasing hormone on ACTH, cortisol and 13, 14-dihydro-15-keto prostaglandin E2 in patients with diabetes insipidus before and after captopril treatment.

A corticotropin-releasing hormone (CRH) test was performed on 7 patients with central diabetes insipidus (DI) and on 7 healthy subjects. The test was repeated on the patients with DI after 3 days of oral treatment with captopril at a dose of 100 mg daily. No significant difference in the responses of plasma ACTH and cortisol to CRH between the patients and the controls was found. The short-term captopril treatment resulted in a significant decrease of both basal and CRH- stimulated ACTH and cortisol levels in the patients with DI. CRH did not induce any changes in the stable metabolite of prostaglandin E2 13, 14-dihydro-15-keto-prostaglandin E2 (PGE2-M) in the patients with DI before or after the captopril treatment. The results obtained suggest that vasopressin is not an obligatory factor for a normal ACTH response to CRH. Angiotensin II (A II) is involved in the regulation of ACTH. This study confirmed our previous data showing the lack of any specific effect of CRH on PGE2 production.[1]

References

  1. Effects of corticotropin-releasing hormone on ACTH, cortisol and 13, 14-dihydro-15-keto prostaglandin E2 in patients with diabetes insipidus before and after captopril treatment. Zacharieva, S., Andreeva, M., Orbetzova, M., Wippermann, M., Mucha, I., Andonova, K., Sheitanova, S. Prostaglandins Leukot. Essent. Fatty Acids (1996) [Pubmed]
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