Modulation of pacemaker activity of sinoatrial node cells by electrical load imposed by an atrial cell model

Eiichi Watanabe, H. Honjo, T. Anno, M. R. Boyett, I. Kodama, J. Toyama

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

To investigate the electrotonic modulation of sinoatrial (SA) node pacemaker activity by atrial muscle, single or multiple (2-7) SA node cells isolated from rabbit hearts were connected to a membrane model [resistance- capacitance (R-C) circuit] of an atrial cell through an external circuit that mimics the gap junctional conductance (G(c)) between cells. When G(c) was 0 nS (uncoupled conditions), all the preparations generated regular and stable spontaneous action potentials with a mean cycle length (SCL) of 263 ± 45 ms (±SD, n = 35). Step increases of G(c) were associated with a progressive prolongation of SCL. At sufficiently high values of G(c), the spontaneous activity became irregular and finally stopped. We defined the threshold G(c) causing an appreciable SCL irregularity as the minimum G(c) at which the ratio of SD to mean of SCL was > 0.3. The threshold G(c) for a single SA node cell was calculated to be 0.58 nS. In the presence of acetylcholine (ACh; 0.05-0.2 μM), the coupling-induced inhibition of spontaneous activity was greatly increased, and the threshold G(c) for a single SA node cell was decreased in a concentration-dependent manner. These findings show that the pacemaker activity of SA node cells is easily inhibited when the cells are coupled to a passive atrial cell model and the inhibition is amplified by ACh. Computer simulation using a modified Oxsoft HEART model indicates that the passive atrial cell model acts as a current sink, imposing a substantial outward current on the SA node cell, and ACh amplifies the effect by activating an additional outward current.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume269
Issue number5 38-5
Publication statusPublished - 01-01-1995
Externally publishedYes

Fingerprint

Sinoatrial Node
Computer Simulation
Action Potentials
Acetylcholine
Rabbits
Muscles

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

@article{60b006e0784e4d39bae9f73eaa278d17,
title = "Modulation of pacemaker activity of sinoatrial node cells by electrical load imposed by an atrial cell model",
abstract = "To investigate the electrotonic modulation of sinoatrial (SA) node pacemaker activity by atrial muscle, single or multiple (2-7) SA node cells isolated from rabbit hearts were connected to a membrane model [resistance- capacitance (R-C) circuit] of an atrial cell through an external circuit that mimics the gap junctional conductance (G(c)) between cells. When G(c) was 0 nS (uncoupled conditions), all the preparations generated regular and stable spontaneous action potentials with a mean cycle length (SCL) of 263 ± 45 ms (±SD, n = 35). Step increases of G(c) were associated with a progressive prolongation of SCL. At sufficiently high values of G(c), the spontaneous activity became irregular and finally stopped. We defined the threshold G(c) causing an appreciable SCL irregularity as the minimum G(c) at which the ratio of SD to mean of SCL was > 0.3. The threshold G(c) for a single SA node cell was calculated to be 0.58 nS. In the presence of acetylcholine (ACh; 0.05-0.2 μM), the coupling-induced inhibition of spontaneous activity was greatly increased, and the threshold G(c) for a single SA node cell was decreased in a concentration-dependent manner. These findings show that the pacemaker activity of SA node cells is easily inhibited when the cells are coupled to a passive atrial cell model and the inhibition is amplified by ACh. Computer simulation using a modified Oxsoft HEART model indicates that the passive atrial cell model acts as a current sink, imposing a substantial outward current on the SA node cell, and ACh amplifies the effect by activating an additional outward current.",
author = "Eiichi Watanabe and H. Honjo and T. Anno and Boyett, {M. R.} and I. Kodama and J. Toyama",
year = "1995",
month = "1",
day = "1",
language = "English",
volume = "269",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "5 38-5",

}

Modulation of pacemaker activity of sinoatrial node cells by electrical load imposed by an atrial cell model. / Watanabe, Eiichi; Honjo, H.; Anno, T.; Boyett, M. R.; Kodama, I.; Toyama, J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 269, No. 5 38-5, 01.01.1995.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Modulation of pacemaker activity of sinoatrial node cells by electrical load imposed by an atrial cell model

AU - Watanabe, Eiichi

AU - Honjo, H.

AU - Anno, T.

AU - Boyett, M. R.

AU - Kodama, I.

AU - Toyama, J.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - To investigate the electrotonic modulation of sinoatrial (SA) node pacemaker activity by atrial muscle, single or multiple (2-7) SA node cells isolated from rabbit hearts were connected to a membrane model [resistance- capacitance (R-C) circuit] of an atrial cell through an external circuit that mimics the gap junctional conductance (G(c)) between cells. When G(c) was 0 nS (uncoupled conditions), all the preparations generated regular and stable spontaneous action potentials with a mean cycle length (SCL) of 263 ± 45 ms (±SD, n = 35). Step increases of G(c) were associated with a progressive prolongation of SCL. At sufficiently high values of G(c), the spontaneous activity became irregular and finally stopped. We defined the threshold G(c) causing an appreciable SCL irregularity as the minimum G(c) at which the ratio of SD to mean of SCL was > 0.3. The threshold G(c) for a single SA node cell was calculated to be 0.58 nS. In the presence of acetylcholine (ACh; 0.05-0.2 μM), the coupling-induced inhibition of spontaneous activity was greatly increased, and the threshold G(c) for a single SA node cell was decreased in a concentration-dependent manner. These findings show that the pacemaker activity of SA node cells is easily inhibited when the cells are coupled to a passive atrial cell model and the inhibition is amplified by ACh. Computer simulation using a modified Oxsoft HEART model indicates that the passive atrial cell model acts as a current sink, imposing a substantial outward current on the SA node cell, and ACh amplifies the effect by activating an additional outward current.

AB - To investigate the electrotonic modulation of sinoatrial (SA) node pacemaker activity by atrial muscle, single or multiple (2-7) SA node cells isolated from rabbit hearts were connected to a membrane model [resistance- capacitance (R-C) circuit] of an atrial cell through an external circuit that mimics the gap junctional conductance (G(c)) between cells. When G(c) was 0 nS (uncoupled conditions), all the preparations generated regular and stable spontaneous action potentials with a mean cycle length (SCL) of 263 ± 45 ms (±SD, n = 35). Step increases of G(c) were associated with a progressive prolongation of SCL. At sufficiently high values of G(c), the spontaneous activity became irregular and finally stopped. We defined the threshold G(c) causing an appreciable SCL irregularity as the minimum G(c) at which the ratio of SD to mean of SCL was > 0.3. The threshold G(c) for a single SA node cell was calculated to be 0.58 nS. In the presence of acetylcholine (ACh; 0.05-0.2 μM), the coupling-induced inhibition of spontaneous activity was greatly increased, and the threshold G(c) for a single SA node cell was decreased in a concentration-dependent manner. These findings show that the pacemaker activity of SA node cells is easily inhibited when the cells are coupled to a passive atrial cell model and the inhibition is amplified by ACh. Computer simulation using a modified Oxsoft HEART model indicates that the passive atrial cell model acts as a current sink, imposing a substantial outward current on the SA node cell, and ACh amplifies the effect by activating an additional outward current.

UR - http://www.scopus.com/inward/record.url?scp=0028807627&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028807627&partnerID=8YFLogxK

M3 - Article

VL - 269

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 5 38-5

ER -