title: Arteriolar occlusion causes independent cellular responses in endothelium and smooth muscle.
abstract: OBJECTIVE
  To test the hypothesis that arteriolar occlusion causes different cellular changes in endothelial and smooth muscle cells.
  
  
  METHODS
  Cheek pouch arterioles (resting diameter 41 +/- 2 microm) of anesthetized hamsters were occluded briefly (<60 seconds) either upstream or downstream from an observation site. Changes in membrane potential and intracellular calcium concentration ([Ca(2+)](i)) of the endothelial or smooth muscle cells were determined by using fluorescence microscopy (ratiometric analysis).
  
  
  RESULTS
  The pressure in the occluded segment decreased by 17.4 +/- 2.6 cm H(2)O during upstream occlusion and increased by 16.8 +/- 6 cm H(2)O during downstream occlusion (n = 5). Upstream occlusion caused vasoconstriction of the occluded segment by 2.4 +/- 0.4 microm, whereas downstream occlusion produced brief vasodilatation by 1.1 +/- 0.2 microm. The endothelial cells hyperpolarized during upstream or downstream occlusion (ratio change: 2.26 +/- 0.24% and 2.39 +/- 0.42%, respectively; p < 0.01, n = 5). There were no changes in endothelial [Ca(2+)](i). The smooth muscle cells depolarized (ratio change: -2.08 +/- 0.14%, n = 5) with an increase in [Ca(2+)](i) (ratio change: 2.92 +/- 0.16%, n = 6) during downstream occlusion. However, there was no detectable change in membrane potential or [Ca(2+)](i) of smooth muscle cells during upstream occlusion. All the changes rapidly recovered when occlusion was released. Responses of an in-situ isolated segment on a side branch revealed conducted dilatory signals caused by the occlusions.
  
  
  CONCLUSIONS
  Our results show that the endothelial and smooth muscle cells respond independently to arteriolar occlusion. The endothelial and smooth muscle cells do not effectively communicate in [Ca(2+)](i) or membrane potential during acute arteriolar occlusion. Hyperpolarizing signals in endothelium cause conducted dilation.
authors.affiliation: Division of Nephrology and Hypertension, Georgetown University Hospital, Washington, DC, USA.
authors.forename: Yifan
authors.initials: Y
authors.lastname: Chen
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Rivers
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000473:pathology* / Q000503:physiopathology; D001160:Arterioles / Q000473:pathology* / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D016764:Cell Polarity; D006224:Cricetinae; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D008564:Membrane Potentials; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000503:physiopathology*; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D002118:Calcium