Document Detail

Urotensin II acutely increases myocardial length and distensibility: potential implications for diastolic function and ventricular remodeling.
MedLine Citation:
PMID:  17701026     Owner:  NLM     Status:  MEDLINE    
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.
Ana Patrícia Fontes-Sousa; Carmen Brás-Silva; Ana Luísa Pires; Daniela Monteiro-Sousa; Adelino F Leite-Moreira
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-08-14
Journal Detail:
Title:  Naunyn-Schmiedeberg's archives of pharmacology     Volume:  376     ISSN:  0028-1298     ISO Abbreviation:  Naunyn Schmiedebergs Arch. Pharmacol.     Publication Date:  2007 Oct 
Date Detail:
Created Date:  2007-11-26     Completed Date:  2008-01-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0326264     Medline TA:  Naunyn Schmiedebergs Arch Pharmacol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  107-15     Citation Subset:  IM    
Department of Physiology, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal.
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MeSH Terms
Analysis of Variance
Diastole* / drug effects
Myocardial Contraction* / drug effects
Nitric Oxide / antagonists & inhibitors,  physiology
Papillary Muscles / drug effects,  physiology
Prostaglandins / physiology
Receptors, G-Protein-Coupled / physiology
Urotensins / pharmacology,  physiology*
Vasoconstrictor Agents / pharmacology
Ventricular Remodeling* / drug effects
Reg. No./Substance:
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

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