Role of Nitric Oxide-cGMP Pathway in Adrenomedullin-Induced Vasodilation in the Rat

We previously reported that adrenomedullin (AM), a potent vasodilator peptide discovered in pheochromocytoma cells, stimulates nitric oxide (NO) release in the rat kidney. To further investigate whether the NO-cGMP pathway is involved in the mechanisms of AM-induced vasodilation, we examined the eff...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 1999-02, Vol.33 (2), p.689-693
Main Authors: Hayakawa, Hiroshi, Hirata, Yasunobu, Kakoki, Masao, Suzuki, Yasuko, Nishimatsu, Hiroaki, Nagata, Daisuke, Suzuki, Etsu, Kikuchi, Kazuya, Nagano, Tetsuo, Kangawa, Kenji, Matsuo, Hisayuki, Sugimoto, Tsuneaki, Omata, Masao
Format: Article
Language:English
Subjects:
Adrenomedullin
Animals
Aorta - drug effects
Aorta - physiology
Biological and medical sciences
Cyclic GMP - physiology
Fundamental and applied biological sciences. Psychology
Kidney - physiology
Male
Nitric Oxide - physiology
Peptides - pharmacology
Rats
Rats, Wistar
Signal Transduction - drug effects
Signal Transduction - physiology
Vasodilation - drug effects
Vasodilation - physiology
Vasodilator Agents - pharmacology
Vertebrates: urinary system
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Summary:We previously reported that adrenomedullin (AM), a potent vasodilator peptide discovered in pheochromocytoma cells, stimulates nitric oxide (NO) release in the rat kidney. To further investigate whether the NO-cGMP pathway is involved in the mechanisms of AM-induced vasodilation, we examined the effects of E-4021, a cGMP-specific phosphodiesterase inhibitor, on AM-induced vasorelaxation in aortic rings and perfused kidneys isolated from Wistar rats. We also measured NO release from the kidneys using a chemiluminescence assay. AM (10 to 10 mol/L) relaxed the aorta precontracted with phenylephrine in a dose-dependent manner. Denudation of endothelium (E) attenuated the vasodilatory action of AM (10 mol/L AMintact (E+) -25.7 +/- 5.2% versus denuded (E-) -7.8 +/- 0.6%, P
ISSN:0194-911X
1524-4563
DOI:10.1161/01.hyp.33.2.689