Ca2+ transients in embryonic chick heart: contributions from Ca2+ channels and the sarcoplasmic reticulum.
In the embryonic mammalian heart, virtually all the Ca2+ available for the Ca2+ transient comes through sarcolemmal Ca2+ influx. However, several studies in avian species indicate that the sarcoplasmic reticulum (SR) is functional relatively early in development. For the present report we studied fura 2 Ca2+ transients elicited by field stimulation in single isolated ventricular myocytes from the day 11 embryonic chick heart to ascertain directly the roles of the SR and Ca2+ channels. A positive staircase phenomenon was observed at higher frequencies of stimulation (1 Hz). Isoproterenol (Iso) increased the peak of the transient in a dose-dependent manner with a maximum increase of 93% in 100 microM Iso. Nifedipine (10 microM) reduced the transient such that is was not observable above background noise. However, Ca2+ transients were visible when the myocytes were stimulated by Iso. These were blocked by approximately 70% with nifedipine, suggesting that most, but not all, of the transient is associated with L-type Ca2+ current. Thus a portion of the transient may result from T-type Ca2+ channels and/or reverse Na+/Ca2+ exchange. Calculations based on integration of the Ca2+ currents and cell volume indicate that as much as one-fourth of the Ca2+ entering via sarcolemmal Ca2+ channels is from T-type channels. Ryanodine at high concentrations (10-100 microM) inhibited the transients by 30%. Both Iso and ryanodine reduced the time to peak, the time constant of the exponential decay, and the total duration of the transients. Depolarizing the myocytes with high KCl induced a large and partially sustained transient when the external solution contained 1.8 mM CaCl2. CaCl2 (10 mM) in the external solution induced large cyclic Ca2+ oscillations. These results suggest that the SR is functional in the embryonic chick heart well before hatching at day 22, although most of the Ca2+ associated with the transient comes through the sarcolemmal Ca2+ channels and possibly reverse Na+/Ca2+ exchange.
Brotto
M A
MA
Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta 30912, USA.
Creazzo
T L
TL
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D002642:Chick Embryo / Q000378:metabolism*; D004558:Electric Stimulation; D004594:Electrophysiology; D006321:Heart / Q000187:drug effects / Q000196:embryology* / Q000502:physiology*; D007545:Isoproterenol / Q000494:pharmacology; D009991:Oscillometry; D011188:Potassium / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D012433:Ryanodine / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000502:physiology*
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D011943:Receptors, Adrenergic, beta; D012433:Ryanodine; D007545:Isoproterenol; D011188:Potassium; D002118:Calcium