Changes in the calcium current of rat heart ventricular myocytes during development.

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Abstract
1. Calcium current (ICa) was recorded in single rat heart cells at two periods during development: (1) at 2-7 days post-partum (neonatal), and (2) at 6-8 weeks (adult). 2. We measured both transient and steady-state components of ICa and could describe ICa in terms of the steady-state activation (d.infin.) and inactivation (f.infin.) parameters, the channel reversal potential (Echannel) and a relative conductance parameter, gr. 3. In adult single cells, the application of ryanodine (10 .mu.M), an agent known to alter the function of the sarcoplasmic reticulum (SR), abolished contraction rapidly and increased ICa. Ryanodine also produced a 13 mV shift in f.infin. towards more positive potentials and altered its slope, while producing a small increase in gr but no effect on d.infin.. In neonatal single cells, ryanodine (10 .mu.M) had no significant effect on contraction, ICa, d.infin., f.infin., or gr. Caffeine (10 mM), a less specific agent widely used to investigate sarcoplasmic reticulum function, had actions similar to those of ryanodine. 4. In adult myocytes, when EGTA (10 or 20 mM) or bis(o-aminophenoxy)ethane-N,N,N'',N"-tetraacetic acid (BAPTA, 10 mM) were included in the pipette solution, contractions were rapidly abolished, while a small (4 mV) shift of f.infin. to more positive potentials was seen. A large additional shift of f.infin. was observed when ryanodine (10 .mu.M) was added to the superfusion solution in the continued presence of EGTA or BAPTA. The alterations of ICa in EGTA (or BAPTA) plus ryanodine were the same as those seen in ryanodine alone. In neonatal cells, in contrast, when EGTA or BAPTA were included in the pipette solution we observed only a small effect on f.infin. and the application of ryanodine had no effect. 5. Electron micrographs of our preparations show that the dissociated adult cells have sharp sarcolemmal borders, fully developed sarcomeres with T-tubules and sarcoplasmic reticulum membranes. In contrast, the neonatal cells that we use have few of these intracellular structures. Our observations in these preparations are consistent with the work of others (e.g. Penefsky, 1974; Hirakow and Gotoh, 1975; Ishikawa and Yamada, 1975; Legato, 1975; Hoerter, Mazet and Vassort, 1981). 6. Our data suggest that fully developed sarcoplasmic reticulum in rat heart cells can affect ICa. We discuss these results in terms of two possible explanations: (1) a physical link between the sarcolemmal (SL) calcium channel and the sarcoplasmic reticulum calcium-release channel (via spanning proteins.sbd.foot processes.sbd.or linking proteins) and (2) an intracellular Ca2+ concentration-([Ca2+]i) dependent modulation of ICa. 7. We conclude that some of the differences in ICa measured in rat heart cells during development can be attributed to the development of the sarcoplasmic reticulum and its connections to the T-tubules and sarcolemma via the spanning proteins.

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