SUMMARYK+ channels regulate tone in both the systemic and pulmonary circulations. K+ channel inhibition leads to membrane depolarization, Ca2+ influx and vasoconstriction; K+ channel activation leads to hyperpolarization and vasodilatation. The sulfhydryl oxidant diamide opens K+ channels in pulmonary smooth muscle and acts as a potent vasodilator in perfused lungs. We examined the hypothesis that antioxidants cause constriction and oxidants cause relaxation through their effects on K+ channels in vascular smooth muscle. The oxidant diamide (380 #/M and 3-8 mM) inhibited the reduction of cytochrome C by ferrous sulphate in vitro whilst the antioxidants co-enzyme Qlo (770 /M) and duroquinone (700 uM) increased the rate of reduction. Both antioxidants caused dose-dependent constriction of endothelium-intact and -denuded rat pulmonary artery and aortic rings. This constriction could be reversed by 1 /M diamide. Co-enzyme Qlo and duroquinone (both at 100 /SM) partially inhibited (-30%) whole-cell K+ channel currents and depolarized membranes of isolated pulmonary artery smooth muscle cells recorded using the amphotericinperforated-patch-clamp technique. Diamide (100 /LM) increased whole-cell K+ channel currents and hyperpolarized the membrane. The data suggest that oxidants and antioxidants may modulate vascular tone via an effect on K+ channels.

SUMMARY1. Simultaneous recordings of membrane potential and edge movement were obtained in spontaneously beating chick embryonic myocardial cell aggregates, which are known to behave as an isopotential syncytium.2. The time course of edge movement was similar in different aggregates, and in different regions of the same aggregate.3. Peak amplitude was increased by 10-6 M-ouabain, and by rapid reduction of the external sodium concentration.4. Peak amplitude was decreased during single premature action potentials, but sustained rapid pacing produced an ascending staircase.5. Depolarizing current pulses increased both the amplitude and duration of the contraction, and caused potentiation ofthe next spontaneous beat. Edge displacement during a series of pulses was a monotonic function of membrane potential.6. Edge movement between action potentials (diastolic movement) was well fitted by an exponential with a mean time constant of 69 msec. Diastolic edge movement was due to a weak, slowly decaying contractile force, which was demonstrated in cells grown on a linear-elastic nylon bristle.7. The time course of diastolic edge movement remained constant, or nearly constant, during variations in peak amplitude that resulted from prematurity of the action potential, exposure to 10-6 m-ouabain, spontaneous mechanical alternans, or prolongation of the action potential by current pulses.8. In contrast, reduction of the external sodium concentration produced marked, selective slowing of the diastolic edge movement. Similar slowing occurred during cooling and during staircase. Diastolic edge movement was selectively accelerated when the preceding interbeat interval was prolonged by a hyperpolarizing current pulse.9. The above observations are consistent with the hypothesis that edge displacement is a monotonic function of contractile force.10. The slow relaxation between action potentials probably reflects removal of intracellular calcium across the surface membrane in exchange for sodium. Changes in the rate of calcium removal may play a role in the regulation of contractility in this tissue.

Serum and IgG from four children with transient erythroblastopenia of childhood (TEC) was tested to see what effect it would have on development of erythroid colonies from bone marrow mononuclear cells. Serum and IgG specimens obtained at the time of diagnosis uniformly suppressed erythroid colony development from CFU-E. Washed bone marrow mononuclear cells from a child with TEC failed to grow in the presence of his own serum, but grew normally in the presence of isologous serum. Serum specimens obtained from patients after recovery from TEC had no effect on erythroid colony development. The anemia of TEC appears to be due to transient immune suppression of erythroid colony development.