Chapter 152: Myocardial Contractility

INTRODUCTION

The heart is made up of striated muscle of both atria and ventricles, along with the pacemaker and action-potential conducting tissue. The pacemaker cells of the myocardium have a unique, self-excitatory property, which allows myocardial contractility to occur independently of sympathetic or parasympathetic nervous system input. The intercalated discs allow the fast, uniform, and sequential transmission of electrical activity (action potentials) between myocytes to generate an effective cardiac output to perfuse vital tissue.

Myocardial contraction occurs as a result of cross-bridge formation between two contractile proteins, actin (thin filaments) and myosin (thick filaments). Contractility refers to the rate of myocyte shortening, which occurs when actin and myosin slide to form cross-bridges (Figure 152-1).

The intracellular release of calcium from the sarcoplasmic reticulum facilitates the conformational change in two regulatory proteins (troponin and tropomyosin) to allow the cross-bridge formation between actin and myosin. The initial calcium release from the sarcoplasmic reticulum is triggered by the electrical depolarization of dihydropyridine, voltage-gated calcium channels. As the intracellular calcium concentration increases, it triggers an even greater release of calcium from the sarcoplasmic reticulum via ryanodine, nonvoltage-gated calcium channels.

The overall calcium concentration and rate of release from the sarcoplasmic reticulum determine the strength as well as rate of the contraction. Sympathetic nervous system stimulation (via norepinephrine) activates beta-1 adrenergic receptors, leading to an increase in the intracellular calcium concentration and strength of contraction. In contrast, parasympathetic nervous system stimulation (via acetylcholine) activates M₂ cholinergic receptors, which enhance the Ca²⁺-ATPase activity to pump calcium back into the sarcoplasmic reticulum, thus effectively lowering the intracellular calcium concentration and decreasing the strength and rate of the myocardial contraction.