title: Changes in cell volume induced by ion channel flux in guinea-pig cardiac myocytes.
abstract: 1. The cell width of guinea-pig ventricular myocytes was measured using an optic device during patch-clamp experiments and the relationship between the ion channel flux and changes in cell volume was examined. 2. On superfusing myocytes with 50, 70, 150 and 200% osmotic solutions, the relative cell width changed to 121.1 (n = 4), 110.8 (n = 27), 87.1 (n = 6) and 82.6% (n = 6) of control, respectively. Changes in cell length were less than 2% in these test solutions. 3. The application of 300 nmol/L isoprenaline to myocytes swollen in the 70% hypotonic solution induced a decrease in cell width from 111.2 to 106.2% (n = 13). The application of isoprenaline in the isotonic solution also induced a decrease in cell width to 96.5% in eight of 13 cells. A membrane depolarization of 2-4 mV accompanied the isoprenaline-induced decrease in volume. In the remaining five cells, neither an obvious isoprenaline-induced decrease in volume nor membrane depolarization was observed. Under ruptured whole-cell voltage clamp conditions, the activation of inward isoprenaline-induced Cl- current decreased cell width. 4. Cell width was seen to either decrease or increase when a large outward or inward K+ current, respectively, was induced by shifting the holding potential or by applying 200 mumol/L pinacidil. Under gramicidin-perforated whole-cell clamp conditions, the cell width did not change, even when a large inward K+ current was induced. 5. When the test solution was applied to half of an elongated myocyte by using a micropipette, the cell width increased or decreased in the part exposed to the hypotonic or hypertonic test solutions, respectively. In contrast, in the other half of the elongated myocyte, the cell width responded in the opposite direction. 6. It is concluded that a continuous ionic flux through ion channels is capable of inducing changes in cell volume by generating a localized osmotic gradient across the cardiac sarcolemma.
authors.affiliation: Department of Physiology, Faculty of Medicine, Kyoto University, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Sasaki
authors.forename: M
authors.initials: M
authors.lastname: Takano
authors.forename: T
authors.initials: T
authors.lastname: Mitsuiye
authors.forename: A
authors.initials: A
authors.lastname: Noma
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology; D048429:Cell Size / Q000187:drug effects / Q000502:physiology; D006168:Guinea Pigs; D006352:Heart Ventricles / Q000166:cytology / Q000187:drug effects; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology*; D007545:Isoproterenol / Q000494:pharmacology; D009206:Myocardium / Q000166:cytology*; D009994:Osmolar Concentration; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000494:pharmacology; D016276:Ventricular Function
chemical_list: D002316:Cardiotonic Agents; D007545:Isoproterenol; D011188:Potassium