AJP - Heart and Circulatory Physiology, Vol 259, Issue 2 395-H402, Copyright © 1990 by American Physiological Society
Rest decay of calcium transients and contractility in feline ventricular myocytes
W. H. DuBell and S. R. Houser
Department of Physiology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
To define the respective contributions of sarcoplasmic reticulum Ca2+
release and action potential-dependent Ca2+ influx to the activator Ca2+,
rest decay of the cytosolic free Ca2+ (Ca2+i) transient and contractility
was measured in feline ventricular myocytes loaded with the
Ca2(+)-sensitive fluorescent dye indo-1. Myocytes were stimulated to a
steady state and then rested for periods ranging from 2 to 120 s. Rest
decay was assayed with both resumption of stimulation and rapid
extracellular applications of caffeine. The protocol was then repeated
after exposure to ryanodine. Ryanodine changed the Ca2+i transients during
steady-state stimulation from large, rapidly rising transients starting
near the resting Ca2+i level to small, slowly rising Ca2+i transients
superimposed on an elevated diastolic Ca2+i. Under control conditions the
stimulation- and caffeine-induced Ca2+i transients exhibited slow monotonic
rest decay with similar time constants of decay (180 and 202 s,
respectively, from a representative cell). After ryanodine, the rest decay
of stimulation-induced Ca2+i transients was seemingly no different.
However, no Ca2+i transient could be elicited by caffeine after 15 s of
rest. These results suggest that 1) under normal conditions the primary
source of activator Ca2+ is the sarcoplasmic reticulum, and 2) the rest
decay of contractility seen in feline ventricular myocytes results from
time-dependent loss of Ca2+ from this organelle.
