Cardiomyocyte Morphology and Physiology

This chapter describes the morphology and physiology of the cells that dominate the composition of the working chambers of the fish heart—the atrial and ventricular myocytes. Contraction and relaxation of the fish atrium and ventricle are achieved through communication between, and the coordination of, these cardiomyocytes. Gap junctions provide electrical continuity between myocytes and propagate the electrical impulse that coordinates the firing of myocyte action potentials. The action potential initiates a sequence of events within the myocyte, which couple the electrical changes in the cell membrane with the mechanical contraction of the myofilaments (actin and myosin) through the transient rise and fall of intracellular Ca^{2 +}. This phenomenon is called excitation–contraction coupling (EC coupling). Mechanical connections between cardiomyocytes, like adherens junctions, help transform cellular contractions and relaxations into the coordinated contraction and relaxation of the heart's chambers. The strength and rate of myocyte contraction is determined by the magnitude and rate of cellular Ca^{2 +} cycling and by the Ca^{2 +} sensitivity of the myofilaments. These in turn can be altered by post-translational modifications like phophorylation, by the cellular environment (incl. temperature, pH and energetics), and in the case of myofilament Ca^{2 +} sensitivity, by sarcomere length. This interplay between the Ca^{2 +} cycling and length-dependent mechanisms that contribute to cardiac force may be important for protecting fish heart function in an environment where conditions are variable.