Rested-state contractions and rest potentiation in spontaneously hypertensive rats

To gain further insight into the excitation-contraction coupling mechanisms in hypertrophy, we studied rested-state contractions, rest decay curves, and rest potentiation under different experimental conditions using papillary muscles of spontaneously hypertensive rats (SHR) and age-matched normoten...

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Autores principales: Pérez, Néstor Gustavo, Vila Petroff, Martín Gerardo, Mattiazzi, Alicia Ramona
Formato: Articulo
Lenguaje:Inglés
Publicado: 1993
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Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/122781
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id I19-R120-10915-122781
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Medicina
hypertrophy
myocardial contraction
papillary muscles
rat, inbred SHR
spellingShingle Medicina
hypertrophy
myocardial contraction
papillary muscles
rat, inbred SHR
Pérez, Néstor Gustavo
Vila Petroff, Martín Gerardo
Mattiazzi, Alicia Ramona
Rested-state contractions and rest potentiation in spontaneously hypertensive rats
topic_facet Medicina
hypertrophy
myocardial contraction
papillary muscles
rat, inbred SHR
description To gain further insight into the excitation-contraction coupling mechanisms in hypertrophy, we studied rested-state contractions, rest decay curves, and rest potentiation under different experimental conditions using papillary muscles of spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar and Wistar-Kyoto (WKY) rats. Under constant stimulation at 1.1 Hz, contractility and relaxation were not significantly different in hypertensive when compared with normotensive animals. Rested-state contraction (the first beat after a rest interval of 15 minutes) increased to 159.2 ± 23% and 123.5 ± 7.5% of prerest values in Wistar and WKY rats, respectively, whereas in SHR it did not differ from prerest values (92.8 ± 9.8%). Ryanodine, used to preferentially inhibit sarcoplasmic reticulum function, eliminated the differences in rested-state contractions observed between hypertensive and normotensive rats. Maximal rest potentiation (the first beat after a rest interval of 1 minute) was also significantly higher in Wistar and WKY rats than in SHR. These differences persisted at low extracellular Na⁺, when Ca<sup>2+</sup> efflux via the Na⁺-Ca<sup>2+</sup> exchanger was inhibited. Rest decay curves (the decay in contractility from maximal rest potentiation to rested-state contraction) showed a similar pattern in the three rat strains. The results suggest that the altered inotropic responses of the SHR arise from an alteration in calcium handling by the sarcoplasmic reticulum. Experiments on saponin-skinned trabeculae indicated that fractional calcium release induced by caffeine was significantly reduced in the SHR. We conclude that the altered inotropic response observed in SHR may reflect a diminished release of calcium from the sarcoplasmic reticulum.
format Articulo
Articulo
author Pérez, Néstor Gustavo
Vila Petroff, Martín Gerardo
Mattiazzi, Alicia Ramona
author_facet Pérez, Néstor Gustavo
Vila Petroff, Martín Gerardo
Mattiazzi, Alicia Ramona
author_sort Pérez, Néstor Gustavo
title Rested-state contractions and rest potentiation in spontaneously hypertensive rats
title_short Rested-state contractions and rest potentiation in spontaneously hypertensive rats
title_full Rested-state contractions and rest potentiation in spontaneously hypertensive rats
title_fullStr Rested-state contractions and rest potentiation in spontaneously hypertensive rats
title_full_unstemmed Rested-state contractions and rest potentiation in spontaneously hypertensive rats
title_sort rested-state contractions and rest potentiation in spontaneously hypertensive rats
publishDate 1993
url http://sedici.unlp.edu.ar/handle/10915/122781
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