title: Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans.
abstract: Volume expansion often ameliorates symptoms of orthostatic intolerance; however, the influence of this increased volume on integrated baroreflex control of vascular sympathetic activity is unknown. We tested whether acute increases in central venous pressure (CVP) diminished subsequent responsiveness of muscle sympathetic nerve activity (MSNA) to rapid changes in arterial pressure. We studied healthy humans under three separate conditions: control, acute 10 degrees head-down tilt (HDT), and saline infusion (SAL). In each condition, heart rate, arterial pressure, CVP, and peroneal MSNA were measured during 5 min of rest and then during rapid changes in arterial pressure induced by sequential boluses of nitroprusside and phenylephrine (modified Oxford technique). Sensitivities of integrated baroreflex control of MSNA and heart rate were assessed as the slopes of the linear portions of the MSNA-diastolic blood pressure and R-R interval-systolic pressure relations, respectively. CVP increased approximately 2 mmHg in both SAL and HDT conditions. Resting heart rate and mean arterial pressure were not different among trials. Sensitivity of baroreflex control of MSNA was decreased in both SAL and HDT condition, respectively: -3.1 +/- 0.6 and -3.3 +/- 1.0 versus -5.0 +/- 0.6 units.beat(-1).mmHg(-1) (P < 0.05 for SAL and HDT vs. control). Sensitivity of baroreflex control of the heart was not different among conditions. Our results indicate that small increases in CVP decrease the sensitivity of integrated baroreflex control of sympathetic nerve activity in healthy humans.
authors.affiliation: Dept. of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. charkoudian.nisha@mayo.edu
authors.forename: N
authors.initials: N
authors.lastname: Charkoudian
authors.forename: E A
authors.initials: EA
authors.lastname: Martin
authors.forename: F A
authors.initials: FA
authors.lastname: Dinenno
authors.forename: J H
authors.initials: JH
authors.lastname: Eisenach
authors.forename: N M
authors.initials: NM
authors.lastname: Dietz
authors.forename: M J
authors.initials: MJ
authors.lastname: Joyner
mesh_terms: D000328:Adult; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D002496:Central Venous Pressure / Q000187:drug effects / Q000502:physiology*; D005260:Female; D018475:Head-Down Tilt / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006400:Hematocrit; D006454:Hemoglobins; D006801:Humans; D008297:Male; D018482:Muscle, Skeletal / Q000294:innervation; D009599:Nitroprusside / Q000008:administration & dosage; D010656:Phenylephrine / Q000008:administration & dosage; D012965:Sodium Chloride / Q000008:administration & dosage; D013564:Sympathetic Nervous System / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000008:administration & dosage; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D006454:Hemoglobins; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D012965:Sodium Chloride