title: Na(+)/Ca(2+)-exchange activity regulates contraction and SR Ca(2+) content in rainbow trout atrial myocytes.
abstract: We have used the whole cell configuration of the patch-clamp technique to measure sarcolemmal Ca(2+) transport by the Na(+)/Ca(2+) exchanger (NCX) and its contribution to the activation and relaxation of contraction in trout atrial myocytes. In contrast to mammals, cell shortening continued, increasing at membrane potentials above 0 mV in trout atrial myocytes. Furthermore, 5 microM nifedipine abolished L-type Ca(2+) current (I(Ca)) but only reduced cell shortening and the Ca(2+) carried by the tail current to 66 +/- 5 and 67 +/- 6% of the control value. Lowering of the pipette Na(+) concentration from 16 to 10 or 0 mM reduced Ca(2+) extrusion from the cell from 2.5 +/- 0.2 to 1.0 +/- 0.2 and 0.5 +/- 0.06 amol/pF. With 20 microM exchanger inhibitory peptide (XIP) in the patch pipette Ca(2+) extrusion 20 min after patch break was 39 +/- 8% of its initial value. With 16, 10, and 0 mM Na(+) in the pipette, the sarcoplasmic reticulum (SR) Ca(2+) content was 47 +/- 4, 29 +/- 6, and 10 +/- 3 amol/pF, respectively. Removal of Na(+) from or inclusion of 20 microM XIP in the pipette gradually eliminated the SR Ca(2+) content. Whereas I(Ca) was the same at -10 or +10 mV, Ca(2+) extrusion from the cell and the SR Ca(2+) content at -10 mV were 65 +/- 7 and 80 +/- 4% of that at +10 mV. The relative amount of Ca(2+) extruded by the NCX (about 55%) and taken up by the SR (about 45%) was, however, similar with depolarizations to -10 and +10 mV. We conclude that modulation of the NCX activity critically determines Ca(2+) entry and cell shortening in trout atrial myocytes. This is due to both an alteration of the transsarcolemmal Ca(2+) transport and a modulation of the SR Ca(2+) content.
authors.affiliation: Department of Physiology, Cell Biology and Immunology, Faculty of Science, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain. Leif@cc.uab.es
authors.forename: L
authors.initials: L
authors.lastname: Hove-Madsen
authors.forename: A
authors.initials: A
authors.lastname: Llach
authors.forename: L
authors.initials: L
authors.lastname: Tort
mesh_terms: D000818:Animals; D016275:Atrial Function; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000502:physiology; D004553:Electric Conductivity; D016014:Linear Models; D008564:Membrane Potentials; D009200:Myocardial Contraction / Q000502:physiology*; D009532:Nickel / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D017686:Oncorhynchus mykiss; D018408:Patch-Clamp Techniques; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D012964:Sodium / Q000008:administration & dosage / Q000494:pharmacology; D019831:Sodium-Calcium Exchanger / Q000502:physiology*
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D019831:Sodium-Calcium Exchanger; D002110:Caffeine; C022838:nickel chloride; D009532:Nickel; D012964:Sodium; D009543:Nifedipine; D002118:Calcium