Kw. Spitzer et al., ELECTROTONIC MODULATION OF ELECTRICAL-ACTIVITY IN RABBIT ATRIOVENTRICULAR NODE MYOCYTES, American journal of physiology. Heart and circulatory physiology, 42(2), 1997, pp. 767-776
Electrotonic effects of electrically coupling atrioventricular (AV) no
dal cells to each other and to real and passive models of atrial and v
entricular cells were studied using a technique that does not require
functional gap junctions. Membrane potential was measured in each cell
using suction pipettes. Mutual entrainment of two spontaneously firin
g AV nodal cells was achieved with a junctional resistance (R-j) of 50
0 M Omega, which corresponds to only 39 junctional channels, assuming
a single-channel conductance of 50 pS. Coupling of AV nodal and atrial
cells at R-j of 50 M Omega caused hyperpolarization of the nodal cell
, decreasing its action potential duration and either slowing or block
ing diastolic depolarization in the AV node myocyte. Opposite changes
occurred in the atrial action potential. When AV nodal and ventricular
cells were coupled at R-j of 50 M Omega, nodal diastolic potential wa
s markedly hyperpolarized, and diastolic depolarization was completely
blocked with little change in ventricular diastolic potential. Howeve
r, coupling did elicit marked changes in the action potential duration
of both cells, with prolongation in the nodal cell and shortening in
the ventricular cell. Nodal maximum upstroke velocity was increased by
both atrial and ventricular coupling, as expected from the hyperpolar
ization that occurred. With an R-j of 50 M Omega, spontaneous firing w
as blocked in all single AV nodal pacemaker cells during coupling to a
real or passive model of an atrial or ventricular cell. These results
demonstrate that action potential formation and waveform in a single
AV nodal cell is significantly affected by electrical coupling to othe
r myocytes.