Vagal cardiac function and arterial blood pressure stability

D. Walter Wray, Kevin J. Formes, Martin S. Weiss, Albert Yurvati, Peter B. Raven, Rong Zhang, Xiangrong Shi

Research output: Contribution to journalArticle

41 Citations (Scopus)

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 μg/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.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume281
Issue number5 50-5
StatePublished - 18 Dec 2001

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Arterial Pressure
Blood Pressure
Muscarinic Antagonists
Glycopyrrolate
Lower Body Negative Pressure
Atropine
Tachycardia
Phenylephrine
Cholinergic Agents
Reflex
Controlled Hypotension
Baroreflex
Bradycardia
Thigh
Volunteers
Homeostasis
Hemodynamics
Hypertension
Injections

Keywords

  • Baroreflex gain
  • Glycopyrrolate
  • Lower body negative pressure
  • Phenylephrine
  • Power spectral analysis
  • Suprasystolic occlusion
  • Valsalva maneuver
  • Vasomotion

Cite this

Wray, D. Walter ; Formes, Kevin J. ; Weiss, Martin S. ; Yurvati, Albert ; Raven, Peter B. ; Zhang, Rong ; Shi, Xiangrong. / Vagal cardiac function and arterial blood pressure stability. In: American Journal of Physiology - Heart and Circulatory Physiology. 2001 ; Vol. 281, No. 5 50-5.
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Vagal cardiac function and arterial blood pressure stability. / Wray, D. Walter; Formes, Kevin J.; Weiss, Martin S.; Yurvati, Albert; Raven, Peter B.; Zhang, Rong; Shi, Xiangrong.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 281, No. 5 50-5, 18.12.2001.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Vagal cardiac function and arterial blood pressure stability

AU - Wray, D. Walter

AU - Formes, Kevin J.

AU - Weiss, Martin S.

AU - Yurvati, Albert

AU - Raven, Peter B.

AU - Zhang, Rong

AU - Shi, Xiangrong

PY - 2001/12/18

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N2 - 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 μg/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.

AB - 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 μg/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.

KW - Baroreflex gain

KW - Glycopyrrolate

KW - Lower body negative pressure

KW - Phenylephrine

KW - Power spectral analysis

KW - Suprasystolic occlusion

KW - Valsalva maneuver

KW - Vasomotion

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M3 - Article

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AN - SCOPUS:0035195979

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JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

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