Effect of manipulations of Ca2+ environment on atrial natriuretic factor release.
The effects of Ca2+ on the kinetics of atrial natriuretic factor (ANF) release [measured as immunoreactive cardionatrin (IRC)] were studied on an in vitro, spontaneously beating rat atrial preparation. It was found that ethylene glycolbis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) and Ca2+-free media induced a significant increase in the rate of basal IRC release. Reintroduction of Ca2+ reversed the augmented basal IRC release induced by EGTA and restored mechanical activity. It was also found that the stretch-induced IRC release was independent of extracellular Ca2+ and took place even in the presence of EGTA. The presence of absence of Ca2+ had no apparent effect on ANF processing. In all instances, cardionatrin I (ANF 99-126) was found to be the most abundant peptide released. Morphologically, no obvious differences were observed during either basal or stretch-induced IRC release. These results suggest that, unlike most other endocrine secretory systems, a reduction of cytosolic Ca2+ stimulates basal IRC release. These findings suggest an adaptation of atrial cardiocytes to accomplish their dual role as secretory and contractile cells.
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ML
Department of Pathology, University of Ottawa Heart Institute Research Centre, Ottawa Civic Hospital, Ontario, Canada.
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AJ
D000818:Animals; D016275:Atrial Function; D009320:Atrial Natriuretic Factor / Q000302:isolation & purification / Q000378:metabolism*; D002118:Calcium / Q000494:pharmacology*; D002851:Chromatography, High Pressure Liquid; D004533:Egtazic Acid / Q000494:pharmacology; D006321:Heart / Q000502:physiology*; D006325:Heart Atria / Q000187:drug effects / Q000648:ultrastructure; D066298:In Vitro Techniques; D007700:Kinetics; D008854:Microscopy, Electron; D009200:Myocardial Contraction / Q000187:drug effects; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains
D004533:Egtazic Acid; D009320:Atrial Natriuretic Factor; D002118:Calcium