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Provedor de dados:  BJMBR
País:  Brazil
Título:  Effect of ryanodine on sinus node recovery time determined in vitro
Autores:  Bassani,J.W.M.
Godoy,C.M.G.
Bassani,R.A.
Data:  1999-08-01
Ano:  1999
Palavras-chave:  Sinus node recovery time
Overdrive suppression
Electrical stimulation
Calcium
Sarcoplasmic reticulum
Ryanodine
Resumo:  Evidence has indicated that the sarcoplasmic reticulum (SR) might be involved in the generation of spontaneous electrical activity in atrial pacemaker cells. We report the effect of disabling the SR with ryanodine (0.1 µM) on the sinus node recovery time (SNRT) measured in isolated right atria from 4-6-month-old male Wistar rats. Electrogram and isometric force were recorded at 36.5oC. Two methods for sinus node resetting were used: a) pulse: a single stimulus pulse interpolated at coupling intervals of 50, 65 or 80% of the regular spontaneous cycle length (RCL), and b) train: a 2-min train of pulses at intervals of 50, 65 or 80% of RCL. Corrected SNRT (cSNRT) was calculated as the difference between SNRT (first spontaneous cycle length after stimulation interruption) and RCL. Ryanodine only slightly increased RCL (<10%), but decreased developed force by 90%. When the pulse method was used, cSNRT (~40 ms), which represents intranodal/atrial conduction time, was independent of the coupling interval and unaffected by ryanodine. However, cSNRT obtained by the train method was significantly higher for shorter intervals between pulses, indicating the occurrence of overdrive suppression. In this case, ryanodine prolonged cSNRT in a rate-dependent fashion, with a greater effect at shorter intervals. These results indicate that: a) a functional SR, albeit important for force development, does not seem to play a major role in atrial automaticity in the rat; b) disruption of cell Ca2+ homeostasis by inhibition of SR function does not appear to affect conduction; however, it enhances overdrive-induced depression of sinusal automaticity.
Tipo:  Info:eu-repo/semantics/other
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999000800015
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X1999000800015
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.32 n.8 1999
Direitos:  info:eu-repo/semantics/openAccess
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