Related Content
Search Google Scholar for:
|
|
Science 23 February 1990: Vol. 247. no. 4945, pp. 969 - 973 DOI: 10.1126/science.2154853
|
|
Articles
Science, Vol 247, Issue 4945, 969-973
Copyright © 1990 by American Association for the Advancement of Science
Atrionatriuretic peptide transforms cardiac sodium channels into calcium-conducting channels
LA Sorbera
and
M Morad
Department of Physiology, University of Pennsylvania, Philadelphia 19104-6085.
The atrionatriuretic peptide (ANP) is released from atrial cells in response to increased extracellular fluid volume and reduces sodium absorption by the kidney, thus reducing the blood volume. In this report, ANP suppressed the calcium and sodium currents in rat and guinea pig ventricular myocytes. The suppression of sodium current was caused by enhanced permeability of the sodium channel to calcium without significant changes in the kinetics or the tetrodotoxin sensitivity of the channel. Thus, ANP may regulate the sodium channel by altering its cationic selectivity site to calcium, thereby repressing the sodium current. The suppression of sodium and calcium channels and the resultant depressed excitability of the atrial cells may help to regulate ANP secretion.
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
- N-Terminal Pro-B-Type Natriuretic Peptide Is a Major Predictor of the Development of Atrial Fibrillation: The Cardiovascular Health Study.
- K. K. Patton, P. T. Ellinor, S. R. Heckbert, R. H. Christenson, C. DeFilippi, J. S. Gottdiener, and R. A. Kronmal (2009)
Circulation
120, 1768-1774
| Abstract »
| Full Text »
| PDF »
- Atrial Natriuretic Peptide Frameshift Mutation in Familial Atrial Fibrillation.
- D. M. Hodgson-Zingman, M. L. Karst, L. V. Zingman, D. M. Heublein, D. Darbar, K. J. Herron, J. D. Ballew, M. de Andrade, J. C. Burnett Jr., and T. M. Olson (2008)
N. Engl. J. Med.
359, 158-165
| Abstract »
| Full Text »
| PDF »
- From a pump to a pore: How palytoxin opens the gates.
- D. W. Hilgemann (2003)
PNAS
100, 386-388
| Full Text »
| PDF »
- L-type Ca2+ current as the predominant pathway of Ca2+ entry during INa activation in {beta}-stimulated cardiac myocytes.
- F. DelPrincipe, M. Egger, and E. Niggli (2000)
J. Physiol.
527, 455-466
| Abstract »
| Full Text »
| PDF »
- Exaggerated QT prolongation after cardioversion of atrial fibrillation.
- A. M. J. Choy, D. Darbar, S. Dell'Orto, and D. M. Roden (1999)
J. Am. Coll. Cardiol.
34, 396-401
| Abstract »
| Full Text »
| PDF »
- Ca2+ Flux Through Promiscuous Cardiac Na+ Channels: Slip-Mode Conductance.
- L. F. Santana, A. M. Gómez, and W. J. Lederer (1998)
Science
279, 1027-1033
| Abstract »
| Full Text »
- Atrial Natriuretic Peptide Inhibits Evoked Catecholamine Release by Altering Sensitivity to Calcium.
- S. Kanwal, B. J. Elmquist, and G. J. Trachte (1997)
J. Pharmacol. Exp. Ther.
283, 426-433
| Abstract »
| Full Text »
- cGMP-Dependent Protein Kinase Regulation of the L-Type Ca2+ Current in Rat Ventricular Myocytes.
- K. Sumii and N. Sperelakis (1995)
Circ. Res.
77, 803-812
| Abstract »
| Full Text »
- Modulation of cardiac sodium channels by cAMP receptors on the myocyte surface.
- L. Sorbera and M Morad (1991)
Science
253, 1286-1289
| Abstract »
| PDF »
- Atrionatriuretic peptide and calcium-conducting sodium channels.
- M. Sheets and D. Hanck (1991)
Science
252, 449-452
| PDF »
- Response.
- L. A. SORBERA and M. MORAD (1991)
Science
252, 450-452
| PDF »
|
|