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The role of the sarcoplasmic reticulum in the response of isolated ferret cardiac muscle to beta‐adrenergic stimulation
Author(s) -
Shah N,
Than N,
White E,
Bennett KL,
Orchard CH
Publication year - 1994
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1994.sp003818
Subject(s) - isoprenaline , ryanodine receptor , endoplasmic reticulum , medicine , lusitropy , endocrinology , stimulation , cardiac muscle , chemistry , muscle contraction , contraction (grammar) , ryanodine receptor 2 , inotrope , papillary muscle , biology , diastole , biochemistry , blood pressure
beta‐Adrenergic stimulation of cardiac muscle leads to an increase in the strength of contraction and an abbreviation of its time course. We have investigated the role of the sarcoplasmic reticulum in these changes by monitoring force and cytoplasmic [Ca2+] in ferret papillary muscles, and the Ca2+ current in isolated ferret myocytes, during the application of isoprenaline in the absence and presence of the sarcoplasmic reticulum inhibitor ryanodine (10(‐6) mol/l). Isoprenaline (10(‐6) mol/l) led to a marked increase in the size of both the twitch and Ca2+ transient, and a decrease in their duration. In the presence of ryanodine, application of isoprenaline had no significant effect on either the size or the time course of the twitch. However, the increase in the Ca2+ current in response to isoprenaline was the same in the absence and presence of ryanodine. Increasing bathing [Ca2+] led to a prolongation of both the twitch and the Ca2+ transient. In the presence of ryanodine, increasing bathing [Ca2+] still increased the size, but decreased the duration, of the twitch. These data provide direct evidence that both the inotropic and lusitropic effects of isoprenaline are mediated via the sarcoplasmic reticulum.