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Comparative study of the inhibitory effects of adrenomedullin on angiotensin II contraction in rat conductance and resistance arteries
Ion Haulica
Laboratory of Experimental and Applied Physiology of the Romanian Academy, Romania, ihaulica{at}yahoo.com
Walther Bild
Department of Physiology, University of Medicine and Pharmacy Iasi, Romania
Christian Mihaila
Department of Physiology, University of Medicine and Pharmacy Iasi, Romania
Dragomir N Serban
Department of Physiology, University of Medicine and Pharmacy Iasi, Romania
Lacramioara Serban
Department of Physiology, University of Medicine and Pharmacy Iasi, Romania
Daniela Boisteanu
Department of Physiology, University of Medicine and Pharmacy Iasi, Romania
Teodor Ionita
Laboratory of Experimental and Applied Physiology of the Romanian Academy, Romania
Oana Radasanu
Laboratory of Experimental and Applied Physiology of the Romanian Academy, Romania
Adrenomedullin (ADM), a ubiquitous vasoactive peptide, has been the target of a multitude of studies concerning its effect on the vascular tone. The present work aims at clarifying a series of its interactions with the renin-angiotensin system.
The study uses the rat aorta ring as a model of conductance vessels, with or without vascular endothelium, and the second order branch of rat mesenteric arteries as a model of resistance arteries. Interactions between various concentrations of ADM and angiotensin II (Ang II) were studied, in the presence of L-NAME (a nitric oxide [NO] synthase inhibitor) and methylene blue (MB; a soluble guanylate cyclase inhibitor).
Results point out differences in the mechanism of the inhibitory action of ADM upon Ang II effects in the two vessel types studied. Inhibition of Ang II contraction by ADM involves guanylate cyclase in both cases. However, NO is involved in ADM-induced inhibition of angiotensinergic not in the resistance ones. vasoconstriction only in the conductance arteries, not in the resistance ones.
Key Words: adrenomedullin angiotensin II L-NAME methylene blue guanylate cyclase
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Journal of Renin-Angiotensin-Aldosterone System, Vol. 5, No. 2,
79-83 (2004)
DOI: 10.3317/jraas.2004.014

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