title: Vagal cardiac function and arterial blood pressure stability.
abstract: This study was designed to investigate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability before and after glycopyrrolate or atropine treatment. Changes in R-R interval (RRI) and ABP were assessed in 10 healthy young (age, 22 +/- 1.8 yr) volunteers during graded lower body negative pressure (LBNP) before and after muscarinic cholinergic (MC) blockade. Transient hypertension was induced by phenylephrine (1 microg/kg body wt), whereas systemic hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. Power spectral densities of systolic [systolic blood pressure (SBP)] and diastolic ABP variability were examined. Both antimuscarinic agents elicited tachycardia similarly without significantly affecting baseline ABP. The increase in SBP after phenylephrine injection (+14 +/- 2 mmHg) was significantly augmented with atropine (+26 +/- 2 mmHg) or glycopyrrolate (+27 +/- 3 mmHg) and associated with a diminished reflex bradycardia. The decrease in SBP after cuff deflation (-9.2 +/- 1.2 mmHg) was significantly greater after atropine (-15 +/- 1 mmHg) or glycopyrrolate (-14 +/- 1 mmHg), with abolished reflex tachycardia. LBNP significantly decreased both SBP and RRI. However, after antimuscarinic agents, the reduction in SBP was greater (P < 0.05) and was associated with less tachycardia. Antimuscarinic agents reduced (P < 0.05) the low-frequency (LF; 0.04-0.12 Hz) power of ABP variability at rest. The LF SBP oscillation was significantly augmented during LBNP, which was accentuated (P < 0.05) after antimuscarinic agents and was correlated (r = -0.79) with the decrease in SBP. We conclude that antimuscarinic agents compromised ABP stability by diminishing baroreflex sensitivity, reflecting the importance of vagal cardiac function in hemodynamic homeostasis. The difference between atropine and glycopyrrolate was not significant.
authors.affiliation: Department of Integrative Physiology and Cardiovascular Research Institute, University of North Texas Health Science Center, Fort Worth, Texas 76107, USA.
authors.forename: D W
authors.initials: DW
authors.lastname: Wray
authors.forename: K J
authors.initials: KJ
authors.lastname: Formes
authors.forename: M S
authors.initials: MS
authors.lastname: Weiss
authors.forename: A H
authors.initials: AH
authors.lastname: O-Yurvati
authors.forename: P B
authors.initials: PB
authors.lastname: Raven
authors.forename: R
authors.initials: R
authors.lastname: Zhang
authors.forename: X
authors.initials: X
authors.lastname: Shi
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage; D000328:Adult; D001285:Atropine / Q000008:administration & dosage; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006024:Glycopyrrolate / Q000008:administration & dosage; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008150:Lower Body Negative Pressure; D008297:Male; D018727:Muscarinic Antagonists / Q000008:administration & dosage; D010656:Phenylephrine / Q000008:administration & dosage; D014630:Vagus Nerve / Q000502:physiology*; D014636:Valsalva Maneuver
chemical_list: D000316:Adrenergic alpha-Agonists; D018727:Muscarinic Antagonists; D010656:Phenylephrine; D001285:Atropine; D006024:Glycopyrrolate