Heart Wall - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 329

Table 6.18. Main features of action potentials and cell shortening in unloaded epi-, endo-, and
midmyocardial myocytes (Sources: [ 625 , 633 ]).

Epicardial Midmyocardial Endocardial

myocyte myocyte myocyte

Action potential

Spike-and-dome + + No

configuration
Duration Shortest Longest

Peak time Longest

Ca 2 + carriers

Ca 2 + influx onset Similar time

Ca 2 + level decay rate

++ + +

SR Ca 2 + content Largest Smallest

Ca V 1.2 Similar density

SERCA ++ + +

NCX Similar density

Cell shortening

Contraction onset Shortest Greatest

Peak time Shortest Longest

Relaxation Fastest

6.6 Excitation-Contraction Coupling

Cyclic blood ejection from cardiac ventricules arises from the synergy between heart
electrical and mechanical functions. Myocardium contraction and relaxation are
influenced by many governing parameters, such as intracellular ion concentrations
and membrane potential, in addition to pre- and afterload and direction and velocity
of movement [ 634 ].
The structure that enables rapid contraction and relaxation of cardiomyocytes is
the connection between transverse tubules and terminal cisternae of the sarcoplas-
mic reticulum. Sodium and calcium channels, Na + -Ca 2 + exchangers, and Na + -K +
pumps aggregate on the T-tubular membranes and colocalize with ryanodine-
sensitive Ca 2 + channels clustered on the sarcoplasmic reticulum membrane. In par-
ticular, many tens of Ca V 1.2 channels and RyRs form couplons that couple
sarcolemmal action potential to release of Ca 2 + messenger (Ca 2 + spike) by the
sarcoplasmic reticulum.
Calcium ions in clefts between transverse tubules and terminal cisternae, i.e.,
in dyad clefts, 66 bind to regulatory calmodulin sites on the cytosolic domains of
Ca V 1.2 channels and rapidly, but partially, inactivate the channels terminating the

66 The so-called dyad is constituted by a T-tubule and a single terminal cisterna.