Activation of contraction in cat ventricular myocytes: Effects of low Cd2+ concentration and temperature

J. Andrew Wasserstrom*, Ana Maria Vites

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


The effects of Cd2+ (20 μM) and different bath temperatures were used to study the contributions of two separate triggering mechanisms, L-type Ca2+ current (I(Ca)) and reverse mode Na+/Ca2+ exchange, to excitation- contraction (E-C) coupling in cat ventricular myocytes. Ionic currents and cell shortening were studied with patch pipettes filled with K+-containing internal solution and discontinuous ('switch') voltage clamp. Superfusion with Cd2+ blocked cell shortening that closely mirrored the block of I(Ca); the voltage dependence of Cd2+-induced reduction in contraction was bell- shaped, displaying minima at test potentials below -10 mV and above +50 mV and a maximum at about +20 mV. Cd2+-insensitive cell shortening was blocked by ryanodine (10 μM) and Ni2+ (4-5 mM). When an action potential was used as the command waveform for the voltage clamp (action potential clamp), Cd2+ reduced contraction to ~60 ± 7% of control cell shortening (n = 7). The remaining contraction was blocked by ryanodine and Ni2+. Superfusion with nifedipine (10 μM) caused nearly identical effects to Cd2+. The voltage dependence of contraction was sigmoidal at temperatures above 34°C but bell-shaped below 30°C. When Cd2+ was added to superfusate, contraction was abolished at 25°C (to 6 ± 3% of control) but reduced only modestly at 34°C (to 65 ± 13% of control, test potential + 10 mV, n = 4, P < 0.01). These results indicate that 1) there is a component of contraction that is sensitive to I(Ca) antagonists, and the block is equivalent with either organic or inorganic antagonists; 2) the contribution of Na+/Ca2+ exchange to triggering of contraction under our experimental conditions is fairly linear throughout the entire voltage range tested; 3) the contribution of I(Ca) is superimposed on this background component contributed by the Na+/Ca2+ exchanger; and 4) triggering via the exchanger is temperature- dependent, providing a major contribution at physiological temperatures but failing at temperatures below 30°C in a nearly all-or-none fashion.

Original languageEnglish (US)
Pages (from-to)H488-H498
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number2 46-2
StatePublished - Aug 1999


  • Calcium current
  • Na/Ca exchange
  • Nickel
  • Nifedipine
  • Ryanodine

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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