Circulation Research, Vol 65, 600-606, Copyright © 1989 by American Heart Association

ARTICLES

Calcium, its role in isoproterenol-stimulated atrial natriuretic peptide secretion by superfused rat atria

RJ Schiebinger
Department of Medicine, Wayne State University, Detroit, Michigan.

The beta-adrenergic agonist isoproterenol stimulates immunoreactive atrial natriuretic peptide (IR-ANP) secretion by superfused rat atria in vitro. beta-Adrenergic agonists alter the cellular handling of calcium, which culminates in a rise in the systolic calcium concentration. This is achieved by increasing calcium influx through voltage-dependent calcium channels and by increasing the storage pool of calcium in the sarcoplasmic reticulum (SR). We therefore asked the question whether isoproterenol-stimulated IR-ANP secretion was dependent on the protein kinase A-induced rise in systolic calcium or was due to a direct effect of protein kinase A activation. Isolated rat left atria paced at 3 Hz were superfused in vitro. IR-ANP secretion was determined by radioimmunoassay of timed collections of the superfusate. Superfusion with 0.1 microM isoproterenol or 0.5 mM dibutyryl cyclic AMP increased IR-ANP secretion twofold. Stimulated IR-ANP secretion was lowered to near baseline by lowering the buffer calcium concentration from 1.8 to 0.2 mM or by adding to the superfusate 10 microM nitrendipine (a calcium-channel blocker) or 1 microM ryanodine (an inhibitor of SR calcium release). Superfusion of nonbeating, electrically quiescent left atria with 0.1 microM isoproterenol failed to stimulate IR-ANP secretion. We conclude: 1) Isoproterenol-stimulated IR-ANP secretion is dependent on calcium influx through voltage- dependent calcium channels and on the release of calcium from the SR. 2) Enhanced calcium influx alone is not adequate to maintain isoproterenol-stimulated IR-ANP secretion. 3) The SR appears to be the primary source of calcium for isoproterenol-stimulated IR-ANP secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				J. Y. Jin, J. F. Wen, D. Li, and K. W. Cho Osmoregulation of atrial myocytic ANP release: osmotransduction via cross-talk between L-type Ca2+ channel and SR Ca2+ release Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2004; 287(5): R1101 - R1109. [Abstract] [Full Text] [PDF]

				A Luchner and H Schunkert Interactions between the sympathetic nervous system and the cardiac natriuretic peptide system Cardiovasc Res, August 15, 2004; 63(3): 443 - 449. [Abstract] [Full Text] [PDF]

				D. Li, J. F. Wen, J. Y. Jin, H. Jin, H. S. Ann, S. Z. Kim, S. H. Kim, H. S. Lee, and K. W. Cho Histamine inhibits atrial myocytic ANP release via H2 receptor-cAMP-protein kinase signaling Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2003; 285(2): R380 - R393. [Abstract] [Full Text] [PDF]

				X. Cui, J. F. Wen, J. Y. Jin, W. X. Xu, S. Z. Kim, S. H. Kim, H. S. Lee, and K. W. Cho Protein kinase-dependent and Ca2+-independent cAMP inhibition of ANP release in beating rabbit atria Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2002; 282(5): R1477 - R1489. [Abstract] [Full Text] [PDF]

				J. F. Wen, X. Cui, J. S. Ahn, S. H. Kim, K. H. Seul, S. Z. Kim, Y. K. Park, H. S. Lee, and K. W. Cho Distinct roles for L- and T-type Ca2+ channels in regulation of atrial ANP release Am J Physiol Heart Circ Physiol, December 1, 2000; 279(6): H2879 - H2888. [Abstract] [Full Text] [PDF]

				D. J. Church, M. C. Rebsamen, D. Morabito, V. van der Bent, M. B. Vallotton, and U. Lang Role of cell contractions in cAMP-induced cardiomyocyte atrial natriuretic peptide release Am J Physiol Heart Circ Physiol, January 1, 2000; 278(1): H117 - H125. [Abstract] [Full Text] [PDF]

				P. Tavi, M. Laine, S. Voutilainen, P. Lehenkari, O. Vuolteenaho, H. Ruskoaho, and M. Weckstrom Potentiation of stretch-induced atrial natriuretic peptide secretion by intracellular acidosis Am J Physiol Heart Circ Physiol, July 1, 1999; 277(1): H405 - H412. [Abstract] [Full Text] [PDF]