Entrained ion transport systems generate the membrane component of chaotic agonist-induced vasomotion.

Abstract

We have analyzed the contribution of membrane ion transport systems to chaotic vasomotion induced by histamine in isolated rabbit ear resistance arteries. Dynamic complexity was monitored as a fractal correlation dimension that provides an estimate of the minimum number of control variables contributing to an irregular time series and generally took a value between 2 and 4. A distinct subcomponent of the overall oscillatory activity (frequency approximately 0.06 Hz) was selectively suppressed by blockade of Ca(2+)-activated K+ channels (KCa) with tetraethylammonium, Ca(2+)-activated Cl- channels with low extracellular Cl- concentration and niflumic acid, the Na(+)-K+ adenosine-triphosphatase (ATPase) with ouabain, and Na+/Ca2+ exchange with low-Na+ buffer. Each of these interventions caused a fall in average fractal dimension to a value < 2, whereas inhibition of voltage-dependent K+ channels with 4-aminopyridine or the Ca(2+)-ATPase extrusion pump with vanadate were without effect on the form and complexity of the vasomotion. There was no systematic correlation between the changes in fractal dimension induced by the various interventions and their effects on perfusion pressure. Our findings suggest that nonlinearity in the kinetics of multiple coupled ion transport systems leads to entrainment and the emergence of a composite membrane oscillator, thus accounting for the low fractal dimension of the vasomotion observed in these arteries.