title: Verapamil and aspirin modulate platelet-mediated vasomotion in arterial segments with intact or disrupted endothelium.
abstract: OBJECTIVE
  This study was designed to examine the effects of verapamil and aspirin, which decrease thromboxane A2 and serotonin release, on the modulation of vascular tone by platelets.
  
  
  BACKGROUND
  Aggregating platelets cause constriction of de-endothelialized arterial segments through thromboxane A2 and serotonin release. These cells cause relaxation of arterial segments with intact endothelium through release of the endothelium-derived relaxing factor.
  
  
  METHODS
  Healthy subjects were given either no drug, verapamil or aspirin for > or = 5 days before their platelets were obtained. The effects of platelets obtained from subjects before and after treatment with aspirin or verapamil on the tone of rat aortic rings were determined.
  
  
  RESULTS
  As expected, control platelets (before verapamil or aspirin treatment) induced concentration-dependent relaxation of rat aortic rings with intact endothelium and a concentration-dependent contraction of de-endothelialized rings. Verapamil treatment enhanced (p < 0.02) the platelet-mediated relaxation in rings with intact endothelium and abolished platelet-mediated constriction (p < 0.01) in the de-endothelialized rings. Aspirin treatment also abolished (p < 0.05) platelet-mediated constriction of the de-endothelialized rings. The de-endothelialized rings contracted normally in response to the synthetic thromboxane A2 analogue U46,619, as well as to serotonin, indicating that the vascular smooth muscle response to thromboxane A2 and serotonin was intact.
  
  
  CONCLUSIONS
  This study provides evidence for the modulation of platelet-mediated vasoconstriction of de-endothelialized arterial segments by prior treatment of subjects with verapamil or aspirin. In clinical syndromes characterized by endothelial dysfunction or disruption, treatment with verapamil or aspirin may modify platelet-vessel wall interactions.
authors.affiliation: Division of Cardiology, University of Florida College of Medicine, Gainesville 32610-0277.
authors.forename: E
authors.initials: E
authors.lastname: Raymenants
authors.forename: B
authors.initials: B
authors.lastname: Yang
authors.forename: F
authors.initials: F
authors.lastname: Nicolini
authors.forename: P
authors.initials: P
authors.lastname: Behrens
authors.forename: D
authors.initials: D
authors.lastname: Lawson
authors.forename: J L
authors.initials: JL
authors.lastname: Mehta
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000502:physiology; D001241:Aspirin / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D002469:Cell Separation; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D010974:Platelet Aggregation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D014655:Vascular Resistance / Q000187:drug effects* / Q000502:physiology; D014700:Verapamil / Q000494:pharmacology*
chemical_list: D014700:Verapamil; D001241:Aspirin