title: Evidence for involvement of central vasopressin V1b and V2 receptors in stress-induced baroreflex desensitization.
abstract: OBJECTIVE
  It is well recognized that vasopressin modulates the neurogenic control of the circulation. Here, we report the central mechanisms by which vasopressin modulates cardiovascular response to stress induced by immobilization.
  
  
  METHODS
  Experiments were performed in conscious male Wistar rats equipped with radiotelemetric device for continuous measurement of haemodynamic parameters: systolic and diastolic BP and heart rate (HR). The functioning of the spontaneous baro-receptor reflex (BRR) was evaluated using the sequence method and the following parameters were evaluated: BRR sensitivity (BRS) and BRR effectiveness index (BEI).
  
  
  RESULTS
  Under baseline physiological conditions intracerebroventricular injection of 100 and 500 ng of selective non-peptide V1a or V1b or V2 receptor antagonist did not modify BP, HR and BRR. Rats exposed to 15 min long stress by immobilization exhibited increase of BP, HR, reduction of BRS and no change in BEI. Pretreatment of rats with V1a receptor antagonist did not modulate the BP, HR, BRS and BEI response to stress. Pretreatment of rats with V1b receptor and V2 receptor antagonist, at both doses, prevented BRR desensitization and tachycardia, but failed to modulate stress-induced hypertension.
  
  
  CONCLUSIONS
  Vasopressin by the stimulation of central V1b- and V2-like receptors mediates stress-induced tachycardia and BRR desensitization. If these mechanisms are involved, BRR desensitization in heart failure and hypertension associated with poor outcome, they could be considered as novel targets for cardiovascular drug development.
authors.affiliation: Faculty of Dentistry, University of Belgrade, Belgrade, Republic of Serbia.
authors.forename: Sanja
authors.initials: S
authors.lastname: Milutinović-Smiljanić
authors.forename: Olivera
authors.initials: O
authors.lastname: Šarenac
authors.forename: Maja
authors.initials: M
authors.lastname: Lozić-Djurić
authors.forename: David
authors.initials: D
authors.lastname: Murphy
authors.forename: Nina
authors.initials: N
authors.lastname: Japundžić-Žigon
mesh_terms: D052636:Allostasis / Q000187:drug effects; D000818:Animals; D014151:Anti-Anxiety Agents / Q000008:administration & dosage / Q000627:therapeutic use; D065092:Antidiuretic Hormone Receptor Antagonists; D017704:Baroreflex / Q000187:drug effects; D002552:Cerebral Ventricles / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D006973:Hypertension / Q000209:etiology / Q000517:prevention & control; D007276:Injections, Intraventricular; D008297:Male; D009419:Nerve Tissue Proteins / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D010865:Pilot Projects; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D017483:Receptors, Vasopressin / Q000819:agonists / Q000378:metabolism*; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000187:drug effects; D013315:Stress, Psychological / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control; D013610:Tachycardia / Q000209:etiology / Q000517:prevention & control; D014667:Vasopressins / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D014151:Anti-Anxiety Agents; D065092:Antidiuretic Hormone Receptor Antagonists; D009419:Nerve Tissue Proteins; D017483:Receptors, Vasopressin; C582099:V2 vasopressin receptor, rat; D014667:Vasopressins