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Contractile effects of ghrelin and expression of its receptor GHS-R1a in normal and hypertrophic myocardium [Efeitos contrácteis da grelina e expressão do seu receptor GHS-R1a no miocárdio normal e hipertrófico]

Title
Contractile effects of ghrelin and expression of its receptor GHS-R1a in normal and hypertrophic myocardium [Efeitos contrácteis da grelina e expressão do seu receptor GHS-R1a no miocárdio normal e hipertrófico]
Type
Article in International Scientific Journal
Year
2005
Authors
Soares, JB
(Author)
Other
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Rocha-Sousa A
(Author)
FMUP
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Castro-Chaves P
(Author)
FMUP
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Henriques-Coelho, T
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FMUP
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Roncon-Albuquerque R Jr
(Author)
FMUP
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Leite-Moreira AF
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FMUP
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Journal
Vol. 24 No. 11
Pages: 1235-1242
ISSN: 0870-2551
Indexing
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Authenticus ID: P-007-EFE
Abstract (EN): Introduction: Ghrelin, isolated in 1999, is an endogenous ligand for the growth hormone secretagogue receptor (GHS-R1a). Recent studies suggest that it may influence the function of normal and failing hearts. Nonetheless, it has been difficult to differentiate its effects on the intrinsic properties of the myocardium from the secondary effects resulting from growth hormone release and vasomotor action. This study investigated the contractile effects of ghrelin and expression of its receptor GHS-R1a in normal and hypertrophic myocardium. Methods: Adult Wistar rats randomly received monocrotaline (MCT; n = 9; 60 mg/kg, sc) or vehicle (n = 7; 1 ml/kg). Three weeks later, after right ventricular (RV) hemodynamic evaluation, the effects of 10-6 M of a pentapeptide active fragment of ghrelin (fG) were tested on contractile parameters of RV papillary muscles (Normal, n = 7; MCT, n = 9). GHS-R1a mRNA expression was estimated in RV transmural free-wall samples (Normal, n = 7; MCT, n = 9), using real-time RT-PCR. Results: In the Normal group, fG reduced active tension (AT), maximum velocity of tension rise (dT/dtmax) and maximum velocity of tension decline (dT/dtmin), by 27.9 ± 4.0%, 28.5 ± 6.7% and 21.4 ± 4.2% respectively. In the MCT group, fG reduced AT, dT/dtmax and dT/dtmin, by 24.1 ± 6.3%, 24.3 ± 6.5% and 24.5 ± 6.1% respectively. GHS-R1a mRNA expression was similar in the two groups (Normal: 2.3*10 5±5.4*104; MCT: 3.0*10 5±1.1*105; p > 0.05). Conclusion: This study shows that ghrelin has negative inotropic and lusitropic effects. These effects and expression of its receptor are preserved in RV hypertrophy, suggesting that ghrelin may be a new target in progression to heart failure.
Language: English
Type (Professor's evaluation): Scientific
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