title: Does the endothelium abolish or promote arterial vasomotion in rat mesenteric arteries? Explanations for the seemingly contradictory effects.
abstract: OBJECTIVE
  Vasomotion consists in cyclic oscillations of the arterial diameter induced by the synchronized activity of the smooth muscle cells. So far, contradictory results have emerged in the literature about the role of the endothelium in the onset and maintenance of vasomotion. Here our aim is to understand how the endothelium may either abolish or promote vasomotion.
  
  
  RESULTS
  We investigate rat mesenteric arterial strips stimulated with phenylephrine (PE). Our results show that the endothelium is not necessary for vasomotion. However, when the endothelium is removed, the PE concentration needed to induce vasomotion is lower and the rhythmic contractions occur for a narrower range of PE concentrations. We demonstrate that endothelium-derived relaxing products may either induce or abolish vasomotion. On the one hand, when the strip is tonically contracted in a nonoscillating state, an endothelium-derived relaxation may induce vasomotion. On the other hand, if the strip displays vasomotion with a medium mean contraction, a relaxation may induce a transition to a nonoscillating state with a small contraction.
  
  
  CONCLUSIONS
  Our findings clarify the role of the endothelium on vasomotion and reconcile the seemingly contradictory observations reported in the literature.
authors.affiliation: Laboratory of Cell Biophysics, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland. dominique.seppey@epfl.ch
authors.forename: Dominique
authors.initials: D
authors.lastname: Seppey
authors.forename: Roger
authors.initials: R
authors.lastname: Sauser
authors.forename: Michèle
authors.initials: M
authors.lastname: Koenigsberger
authors.forename: Jean-Louis
authors.initials: JL
authors.lastname: Bény
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Meister
mesh_terms: D000818:Animals; D001030:Apamin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D045462:Endothelium-Dependent Relaxing Factors / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008638:Mesenteric Arteries / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D010507:Periodicity; D010656:Phenylephrine / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000037:antagonists & inhibitors / Q000378:metabolism; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D045462:Endothelium-Dependent Relaxing Factors; D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D026902:Potassium Channel Blockers; D051640:Small-Conductance Calcium-Activated Potassium Channels; D014662:Vasoconstrictor Agents; D009599:Nitroprusside; D010656:Phenylephrine; D001030:Apamin; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester