Volume changes in cardiac ventricles from Aplysia brasiliana upon exposureto hyposmotic shock

We investigated the possible role of ion channels and transporters in cell volume control using Aplysia brasiliana ventricular tissues exposed to a 26 % hyposmotic shock, by assessing changes in wet weight, intracellular water and ionic contents. Thirty minutes after the shock, the wet weight of isol ated ventricles increase about 20% above control levels and then attain nea r original weight within 60 min after the shock. At the time when the wet w eight returned to control values, intracellular water and KCl contents are decreased by 22 and 20%, respectively. The K+ channel blockers, 4-AP and TE A, but not the cotransport blockers, hydrochlorothiazide and furosemide, gr eatly affect the magnitude of wet weight gain and the time course of weight recovery, indicating that KCI loss occur through conductive pathways. Intr acellular recordings performed on ventricular myocytes during exposure to t he osmotic shock showed an immediate membrane hyperpolarization and blockad e of spontaneous electrical activity; diastolic membrane potential recover over time and spontaneous action potentials are completely restored 60 min after the hyposmotic shock. Because significant weight loss is observed dur ing the exposure of ventricular tissues to 26% hypo-ionic, but isosmotic sa line, it is suggested that ventricular volume restoration is accomplished b y two distinct but simultaneously occurring processes: a volume-dependent a nd a volume-independent mechanism. Because wet weight restoration is comple tely prevented by exposing ventricular tissue to a Ca2+-free hyposmotic sol ution, we postulate that both processes involved in A. brasiliana ventricul ar weight restoration are Ca2+-dependent mechanisms. (C) 2000 Elsevier Scie nce Inc. All rights reserved.