title: Diminished baroreflex control of heart rate responses in otoconia-deficient C57BL/6JEi head tilt mice.
abstract: The maintenance of stable blood pressure during postural changes is known to involve integration of vestibular and cardiovascular central regulatory mechanisms. Sensory activity in the vestibular system plays an important role in cardiovascular regulation. The purpose of this study was to determine the role of vestibular gravity receptors in normal baroreflex function. Baroreflex heart rate (HR) responses to changes in blood pressure (BP) in otoconia-deficient head tilt (het) mice (n = 8) were compared with their wild-type littermates (n = 12). The study was carried out in conscious male mice chronically implanted with arterial and venous catheters for recording BP and HR and for the infusion of vasoactive drugs. Resting HR was higher in the het mice (661 +/- 13 beats/min) than in the wild-type mice (579 +/- 20 beats/min). BP was comparable in the het (113 +/- 4 mmHg) and wild-type mice (104 +/- 4 mmHg). The slopes of reflex decreases in HR in response to phenylephrine (PE) were blunted in the het mice (-5.5 +/- 1.5 beats x min(-1) x mmHg(-1)) compared with the wild-type mice (-8.5 +/- 0.9 beats x min(-1) x mmHg(-1)). Likewise, reflex tachycardic responses to decreases in BP with sodium nitroprusside (SNP) were significantly blunted in the het mice (-0.8 +/- 0.3 beats x min(-1) x mmHg(-1)) versus the wild-type mice (-2.2 +/- 0.6 beats x min(-1) x mmHg(-1)). Frequency-domain analysis of the HR variability suggests that under resting conditions, parasympathetic contribution was lower in the het versus wild-type mice. Mapping of the expression of immediate-early gene product, c-Fos, in forebrain and brain stem nuclei in response to a BP challenge showed no differences between the wild-type and het mice. These results suggest that tonic activity of gravity receptors modulates and is required for normal function of the cardiac baroreflexes.
authors.affiliation: Dalton Cardiovascular Research Center and Biomedical Sciences, School of Medicine, University of Missouri, Missouri, Columbia, MO 65211, USA.
authors.forename: Baojian
authors.initials: B
authors.lastname: Xue
authors.forename: Karl
authors.initials: K
authors.lastname: Skala
authors.forename: Timothy A
authors.initials: TA
authors.lastname: Jones
authors.forename: Meredith
authors.initials: M
authors.lastname: Hay
mesh_terms: D000818:Animals; D017704:Baroreflex; D001794:Blood Pressure / Q000187:drug effects; D001933:Brain Stem / Q000378:metabolism / Q000503:physiopathology; D002319:Cardiovascular System / Q000503:physiopathology; D000013:Congenital Abnormalities / Q000235:genetics / Q000503:physiopathology; D005730:Ganglionic Blockers / Q000494:pharmacology; D006257:Head; D006339:Heart Rate; D018738:Hexamethonium / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D010037:Otolithic Membrane / Q000002:abnormalities*; D011187:Posture; D016548:Prosencephalon / Q000378:metabolism / Q000503:physiopathology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism
chemical_list: D005730:Ganglionic Blockers; D016760:Proto-Oncogene Proteins c-fos; D018738:Hexamethonium