title: Comparison of aortic and carotid baroreflex stimulus-response characteristics in humans.
abstract: In order to characterize the stimulus-response relationships of the arterial, aortic, and carotid baroreflexes in mediating cardiac chronotropic function, we measured heart rate (HR) responses elicited by acute changes in mean arterial pressure (MAP) and carotid sinus pressure (CSP) in 11 healthy individuals. Arterial (aortic + carotid) baroreflex control of HR was quantified using ramped changes in MAP induced by bolus injection of phenylephrine (PE) and sodium nitroprusside (SN). To assess aortic-cardiac responses, neck pressure (NP) and suction (NS) were applied during PE and SN administration, respectively, to counter alterations in CSP thereby isolating the aortic baroreflex. Graded levels of NP and NS were delivered to the carotid sinus using a customized neck collar device to assess the carotid-cardiac baroreflex, independent of drug infusion. The operating characteristics of each reflex were determined from the logistic function of the elicited HR response to the induced change in MAP. The arterial pressures at which the threshold was located on the stimulus-response curves determined for the arterial, aortic and carotid baroreflexes were not significantly different (72+/-4, 67+/-3, and 72+/-4 mm Hg, respectively, P > 0.05). Similarly, the MAP at which the saturation of the reflex responses were elicited did not differ among the baroreflex arcs examined (98+/-3, 99+/-2, and 102+/-3 mm Hg, respectively). These data suggest that the baroreceptor populations studied operate over the same range of arterial pressures. This finding indicates each baroreflex functions as both an important anti-hypotensive and anti-hypertensive mechanism. In addition, this investigation describes a model of aortic baroreflex function in normal healthy humans, which may prove useful in identifying the origin of baroreflex dysfunction in disease- and training-induced conditions.
authors.affiliation: Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth 76107, USA. scott.smith@utsouthwestern.edu
authors.forename: S A
authors.initials: SA
authors.lastname: Smith
authors.forename: R G
authors.initials: RG
authors.lastname: Querry
authors.forename: P J
authors.initials: PJ
authors.lastname: Fadel
authors.forename: M W
authors.initials: MW
authors.lastname: Weiss
authors.forename: A
authors.initials: A
authors.lastname: Olivencia-Yurvati
authors.forename: X
authors.initials: X
authors.lastname: Shi
authors.forename: P B
authors.initials: PB
authors.lastname: Raven
mesh_terms: D000328:Adult; D001011:Aorta / Q000502:physiology*; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D002339:Carotid Arteries / Q000502:physiology*; D002346:Carotid Sinus / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D010812:Physical Stimulation; D012016:Reference Values; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine