Advertisement

Cellular Mechanisms of Relaxation: Lessons from Frogs, Birds, and Mammals

  • William H. Barry

Abstract

Much progress has been made in the elucidation of the cellular mechanisms of development and relaxation of twitch tension in cardiac muscle. The onset of contraction is preceded by a rise in cytosolic calcium ion concentration, [Ca2+]i [1]. This rise in [Ca2+]i, in mammalian ventricular myocytes appears primarily to be due to release of Ca2+ from intracellular stores contained within the sarcoplasmic reticulum (SR), the release being triggered by influx of extracellular Ca2+ across the sarcolemma via the slow calcium channel during phase 2 of the cardiac action potential. In frog myocardium, little of the Ca2+ involved in excitation-contraction coupling is derived from intracellular stores because of a very sparse SR, and therefore most of the rise in [Ca2+]i occurs because of transsarcolemmal Ca2+ influx via the slow Ca2+ channel and possibly via an electrogenic Na+−Ca2+ exchange [2]. Calcium bound to sarcolemmal sites may also be of importance in the excitation-contraction coupling process [3], possibly by providing a source for Ca2+ influx.

Keywords

Sarcoplasmic Reticulum Slow Phase Caffeine Exposure Initial Rapid Phase Culture Heart Cell 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Fabiato A, Fabiato F (1979). Calcium and cardiac excitation-contraction coupling. Annu Rev Physiol 41: 473–484.PubMedCrossRefGoogle Scholar
  2. 2.
    Horakova M, Vassort G (1979). Na-Ca exchange in the regulation of cardiac contractility. J Gen Physiol 73: 403–424.CrossRefGoogle Scholar
  3. 3.
    Langer GA, Nudd LM (1983). Effects of cations, phospholipases, and neuraminidase on calcium binding to “gas-dissected” membranes from cultured cardiac cells. Circ Res. 53: 482–490.PubMedGoogle Scholar
  4. 4.
    Carafoli, E (1985). The homeostasis of calcium in heart cells. J Mol Cell Cardiol 17: 203–212.PubMedCrossRefGoogle Scholar
  5. 5.
    Miura DS, Biedert S, Barry WH (1981). Effects of calcium overload on relaxation in cultured heart cells. J Mol Cell Cardiol 13: 949–961.PubMedCrossRefGoogle Scholar
  6. 6.
    Barry WH, Pober J, Marsh JD, Frankel SR, Smith TW (1980). Effects of graded hypoxia on contraction of cultured chick embryo ventricular cells. Am J Physiol 239: H651 - H657.PubMedGoogle Scholar
  7. 7.
    Barry WH, Rasmussen CAF Jr, Ishida H, Bridge JHB (1986). External Na-independent Ca extrusion in cultured ventricular cells. J Gen Physiol 88: 393–411, 1986.Google Scholar
  8. 8.
    Grynkiewicz G, Poenie M, Tsien RY (1985). A new generation of Ca2+ indicators with greatly improved fluorescence properties. J Biol Chem 260: 3440–3450.PubMedGoogle Scholar
  9. 9.
    Peeters GA, Hlady V, Bridge JHB, Barry WH (1986). Simultaneous measurement of calcium transients and cell motion in cultured cells. Am J Physiol, (in press).Google Scholar
  10. 10.
    Clusin WT (1981). The mechanical activity of chick embryonic myocardial cell aggregates. J Physiol 320: 149–174.PubMedGoogle Scholar
  11. 11.
    Isenberg G (1982). Ca entry and contraction as studied in isolated bovine ventricular myocytes. Z Naturforsch 37: 502–512.Google Scholar
  12. 12.
    Barry WH, Smith TW (1984). Movement of Ca2+ across the sarcolemma: effects of abrupt exposure to zero external Na concentration. J Mol Cell Cardiol 16: 155–164.PubMedCrossRefGoogle Scholar
  13. 13.
    Lakatta EG, Capogrossi MC, Kort AA, Stern MD (1985). Spontaneous myocardial calcium oscillations: Overview with emphasis on ryanodine and caffeine. Fed Proc 44: 2977–2983.Google Scholar
  14. 14.
    Manasek FJ (1969). Histogenesis of the embryonic myocardium. Am J Cardiol 25: 149–168.CrossRefGoogle Scholar
  15. 15.
    Holland PC (1979). Biosynthesis of the Ca2+ and Mg’-dependent adenosine triphosphatase of sarcoplasmic reticulum in cell cultures of embryonic chick heart. J Biol Chem 254: 7604–7610.PubMedGoogle Scholar
  16. 16.
    Rasmussen CAF Jr, Sutko JL, Barry WH (1987). Effects of ryanodine and caffeine on contractility, membrane voltage, and calcium exchange in cultured heart cells. Circ Res 60: 495–504.PubMedGoogle Scholar
  17. 17.
    Roulet MJ, Mongo KG, Vassort G, Ventura-Clapier R (1979). The dependence of twitch relaxation on sodium ions and on internal Ca2+ stores in voltage clamped frog atrial fibers. Pfluegers Arch 379: 259–268.CrossRefGoogle Scholar
  18. 18.
    Barry WH, Hasin Y, Smith TW (1985). Sodium pump inhibition, enhanced calcium influx via sodium-calcium exchange, and positive inotropic response in cultured heart cells. Circ Res 56: 231–241.PubMedGoogle Scholar
  19. 19.
    Cleeman L, Pizarro G, Morad M (1984). Optical measurements of extra-cellular calcium depletion during a single heart beat. Science 226: 172–177.CrossRefGoogle Scholar
  20. 20.
    Robertson SP, Johnson JD, Potter JD (1981). The time course of Ca’ exchange with cal-modulin, troponin, parvalbumin and myosin in response to transient increases in Ca“. Biophys J 34: 559–569.PubMedCrossRefGoogle Scholar
  21. 21.
    Fabiato A (1983). Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum. Am J Physiol 245: C1 – C14.PubMedGoogle Scholar
  22. 22.
    Fabiato A (1984). Effects of spermine in skinned cardiac cells suggest that mitochondria do not participate in beat-to-beat Ca2+ regulation in intact cardiac cells but control [free Ca2+]. J Gen Physiol 84:37–38a (abstract).Google Scholar

Copyright information

© Martinus Nijhoff Publishing 1987

Authors and Affiliations

  • William H. Barry

There are no affiliations available

Personalised recommendations