Abstract
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 microM) 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 36.5 degree C. 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 ( approximately 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.
Highlights
In the present study, we investigated the role of a functional sarcoplasmic reticulum (SR) in the determination of the clinically used parameter corrected sinus node recovery time (SNRT) (cSNRT), using a previously characterized in vitro approach [6]
We investigated the role of a functional SR in the determination of the clinically used parameter cSNRT, using a previously characterized in vitro approach [6]
SNRT values obtained from the electrogram were considered acceptable only when they indicated sinus node resetting. cSNRT was calculated subtracting the previous mean regular spontaneous cycle length (RCL) from SNRT
Summary
Wistar rats (4-6 months old) and incubated in Krebs-Henseleit solution of the following composition: 122.3 mM NaCl, 4.6 mM KCl, 2.5 mM CaCl2, 1.2 mM KH2PO4, 17.7 mM NaHCO3, 1.2 mM MgSO4, 11.1 mM glucose, pH 7.4, saturated with 95% O2/5% CO2, at 36.5oC. CSNRT values obtained by the pulse method under control conditions were similar regardless of pulse prematurity (45 ± 10, 42 ± 10 and 41 ± 10 ms for intervals of 50, 65 and 80% RCL, respectively). In control experiments a negative relationship between cSNRT and interval was observed, so that cSNRT at the shortest interval (64 ± 10 ms at 50% of RCL) was twice as long as that recorded with the interval closer to RCL (33 ± 4 ms at 80% of RCL) The latter was not significantly different from the values obtained with the pulse method. SR inhibition with ryanodine caused an interval-dependent prolongation of cSNRT (P
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