title: Relating drug-induced changes in carotid artery mechanics to cardiovagal and sympathetic baroreflex control.
abstract: Previous evidence indicates that sensitivity of the baroreflex cardiovagal and sympathetic arms is dissociated. In addition, pharmacologic assessment of baroreflex sensitivity (BRS) has revealed that cardiovagal, but not sympathetic, BRS is greater when blood pressure is increasing versus falling. The origin of this hysteresis is unknown. In this study, carotid artery distensibility and absolute distension (diameter) were assessed to test the hypothesis that vessel mechanics in barosensitive regions affect the BRS of cardiovagal, but not sympathetic, outflow. R-R interval (i.e. time between successive R waves), finger arterial blood pressure, muscle sympathetic nerve activity, and carotid artery dimensions (B-mode imaging) were measured during sequential infusions of sodium nitroprusside (SNP) and phenylephrine (PHE). Systolic and diastolic common carotid artery diameters and pulse pressure were recorded to calculate distensibility of this vessel under each drug condition. Cardiovagal BRS was greater when blood pressure was increasing versus decreasing (p < 0.01). Sympathetic BRS was not affected by direction of pressure change. Distensibility did not differ between SNP and PHE injections. However, compared with SNP, infusion of PHE resulted in larger absolute systolic and diastolic carotid diameters (p < 0.001). Therefore, cardiovagal reflex hysteresis was related to drug-induced changes in common carotid artery diameter but not distensibility. The lack of sympathetic hysteresis in this model suggests a relative insensitivity of this baroreflex component to carotid artery dimensions and provides a possible mechanism for the dissociation between cardiovagal and sympathetic BRS.
authors.affiliation: Department of Community Health Sciences, Brock University, St. Catharines, ON L2S 3A1, Canada. doleary@brocku.ca
authors.forename: Deborah D
authors.initials: DD
authors.lastname: O'Leary
authors.forename: Craig D
authors.initials: CD
authors.lastname: Steinback
authors.forename: Angela D
authors.initials: AD
authors.lastname: Cechetto
authors.forename: Blaine T
authors.initials: BT
authors.lastname: Foell
authors.forename: Jane C
authors.initials: JC
authors.lastname: Topolovec
authors.forename: Adrian W
authors.initials: AW
authors.lastname: Gelb
authors.forename: David F
authors.initials: DF
authors.lastname: Cechetto
authors.forename: J Kevin
authors.initials: JK
authors.lastname: Shoemaker
mesh_terms: D000328:Adult; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries / Q000187:drug effects* / Q000294:innervation / Q000502:physiology; D004548:Elasticity; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000187:drug effects / Q000294:innervation; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology*; D010656:Phenylephrine / Q000008:administration & dosage / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology; D014630:Vagus Nerve / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine