Depolarization of the T tubule membrane
activates the sarcoplasmic reticulum via dihydropyridine receptors (DHPRs),
named for the drug dihydropyridine, which blocks them (Figure 5–7). DHPRs
are voltage-gated Ca2+ channels in the T tubule membrane. In cardiac muscle,
influx of Ca2+ via these channels triggers the release of Ca2+ stored in the
sarcoplasmic reticulum (ie, Ca2+-induced Ca2+ release) by activating the
ryanodine receptor (RyR). The RyR is named after the plant alkaloid ryanodine
that was used in its discovery. The RyR is a ligand-gated Ca2+ channel with Ca2+
as its natural ligand. In skeletal muscle, Ca2+ entry from the extracellular fluid
(ECF) by this route is not required for Ca2+ release. Instead, the DHPR that
serves as the voltage sensor triggers release of Ca2+ from the nearby
sarcoplasmic reticulum via physical interaction with the RyR.
As the heart then proceeds through its normal process
of depolarization, the septum first becomes depolarized;
then the depolarization spreads down to the apex and
back toward the bases of the ventricles. The last portion
of the ventricles to become totally depolarized is the base
of the right ventricle because the base of the left ventricle
is already totally and permanently depolarized.
By : Guyton
