title: Fractal analysis of role of smooth muscle Ca2+ fluxes in genesis of chaotic arterial pressure oscillations.
abstract: We have investigated the role of vascular smooth muscle Ca2+ fluxes in the genesis of chaotic pressure oscillations induced by histamine in isolated resistance arteries from the rabbit ear. The responses exhibited distinct "fast" and "slow" components, with periods of 5-20 s and 1-5 min, respectively, which could be dissociated pharmacologically. The fast subsystem involved ion movements at the cell membrane and was inhibited by both low (< 2 mM) and high (> 5 mM) extracellular Ca2+ concentration ([Ca2+]o) by verapamil (which inhibits voltage-dependent Ca2+ influx) and by charybdotoxin (ChTX) and apamin (which block Ca(2+)-activated K+ channels). In contrast, the slow subsystem was intracellular and was selectively attenuated by ryanodine, which inhibits Ca(2+)-induced Ca2+ release from sarcoplasmic reticulum. The effects of these interventions on the complexity of the responses were quantified by calculating their fractal dimension, a parameter that estimates the minimum number of independent variables contributing to an irregular time series. Its mean value was generally > 2 under control conditions but decreased to < 2 in a concentration-dependent fashion in the presence of verapamil, ChTX, apamin, or ryanodine and when [Ca2+]o was outside the range of 2-3 mM. Each intervention thus removed one dimension of complexity from the mechanisms generating the rhythmic activity. We conclude that the interaction of a fast membrane oscillator, which involves Ca2+ influx, Ca(2+)-activated K+ efflux, and therefore presumably changes in membrane potential, and a slow intracellular oscillator involving Ca2+ sequestration and release from stores is responsible for vascular chaos in our model. The coupling between these subsystems is likely to be mediated by cytosolic [Ca2+].
authors.affiliation: Department of Diagnostic Radiology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom.
authors.forename: T M
authors.initials: TM
authors.lastname: Griffith
authors.forename: D H
authors.initials: DH
authors.lastname: Edwards
mesh_terms: D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers; D015220:Calcium Channels / Q000502:physiology; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D018999:Charybdotoxin; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester; D017711:Nonlinear Dynamics; D009991:Oscillometry; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D011817:Rabbits; D012433:Ryanodine / Q000494:pharmacology*; D012604:Scorpion Venoms / Q000494:pharmacology; D013997:Time Factors; D014700:Verapamil / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D015221:Potassium Channels; D012604:Scorpion Venoms; D018999:Charybdotoxin; D012433:Ryanodine; D001030:Apamin; D006632:Histamine; D001120:Arginine; D014700:Verapamil; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester