| Urotensin II acutely increases myocardial length and distensibility: potential implications for diastolic function and ventricular remodeling. | |
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MedLine Citation:
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PMID: 17701026 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Urotensin II (U-II) is a cyclic peptide that may be involved in cardiovascular dysfunction. In the present study, the acute effects of U-II on diastolic properties of the myocardium were investigated. Increasing concentrations of U-II (10(-8) to 10(-6) M) were added to rabbit papillary muscles in the absence (n = 15) or presence of: (1) damaged endocardial endothelium (EE; n = 9); (2) U-II receptor antagonist, urantide (10(-5) M; n = 7); (3) nitric oxide (NO) synthase inhibitor, N(G)-Nitro-L-Arginine (10(-5) M; n = 9); (4) cyclooxygenase inhibitor, indomethacin (10(-5) M; n = 8); (5) NO synthase and cyclooxygenase inhibitors, N(G)-Nitro-L-Arginine (10(-5) M) and indomethacin (10(-5) M), respectively, (n = 8); or (6) protein kinase C (PKC) inhibitor, chelerythrine (10(-5) M; n = 9). Passive length-tension relations were constructed before and after a single concentration of U-II (10(-6) M; n = 3). U-II concentration dependently decreased inotropy and increased resting muscle length (RL). At 10(-6) M, active tension decreased 13.8 +/- 5.4%, and RL increased to 1.007 +/- 0.001 L/L (max). Correcting RL to its initial value resulted in an 18.1 +/- 3.0% decrease in resting tension, indicating decreased muscle stiffness, which was also suggested by the down and rightward shift of the passive length-tension relation. This effect remained unaffected by EE damage and PKC inhibition. In contrast, the presence of urantide and NO inhibition abolished the effects of U-II on myocardial stiffness, while cyclooxygenase inhibition significantly attenuated them. U-II decreases myocardial stiffness, an effect that is mediated by the urotensin-II receptor, NO, and prostaglandins. This represents a novel mechanism of acute neurohumoral modulation of diastolic function, suggesting that U-II is an important regulator of cardiac filling. |
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Authors:
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Ana Patrícia Fontes-Sousa; Carmen Brás-Silva; Ana Luísa Pires; Daniela Monteiro-Sousa; Adelino F Leite-Moreira |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't Date: 2007-08-14 |
Journal Detail:
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Title: Naunyn-Schmiedeberg's archives of pharmacology Volume: 376 ISSN: 0028-1298 ISO Abbreviation: Naunyn Schmiedebergs Arch. Pharmacol. Publication Date: 2007 Oct |
Date Detail:
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Created Date: 2007-11-26 Completed Date: 2008-01-17 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0326264 Medline TA: Naunyn Schmiedebergs Arch Pharmacol Country: Germany |
Other Details:
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Languages: eng Pagination: 107-15 Citation Subset: IM |
Affiliation:
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Department of Physiology, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Analysis of Variance Animals Diastole* / drug effects Elasticity Humans Male Myocardial Contraction* / drug effects Nitric Oxide / antagonists & inhibitors, physiology Papillary Muscles / drug effects, physiology Prostaglandins / physiology Rabbits Receptors, G-Protein-Coupled / physiology Urotensins / pharmacology, physiology* Vasoconstrictor Agents / pharmacology Ventricular Remodeling* / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Prostaglandins; 0/Receptors, G-Protein-Coupled; 0/UTS2R protein, human; 0/Urotensins; 0/Vasoconstrictor Agents; 10102-43-9/Nitric Oxide; 9047-55-6/urotensin II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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