Distribution of abnormal karyotypes among malformed fetuses detected by ultrasound throughout gestation

The participation of sarcoplasmic reticulum Ca2+ release channels in the activation of Ca(2+)-sensitive K+ currents (IK(Ca)) by cyclic dibutyryl GMP was investigated in smooth muscle cells from the circular layer of guinea-pig gastric fundus. All experiments were performed in the presence of 3 microM nicardipine into the bath and low Ca2+ buffering capacity of the pipette-filling solution (pCa 7.4). Ruthenium red (10 microM) as well as its combination with 10 microM heparin abolished the cyclic GMP-induced activation of IK(Ca), while 10 microM heparin remained ineffective. Ryanodine (10 microM) and the subsequently added 1 microM thapsigargin induced a relatively small increase in IK(Ca) amplitudes. The addition of 10 microM ryanodine to 1 microM thapsigargin-containing bath solution caused a vast increase in IK(Ca). It is hypothesyzed that protein kinase G-induced vectorial Ca2+ flux from the cell bulk and sarcoplasmic reticulum Ca2+ stores toward the plasma membrane is realized by a spontaneous Ca(2+)-induced Ca2+ release from a superficially situated Ca2+ store.