A reduction of cytosolic Ca2+ stimulates basal atrial natriuretic factor release in rat atrial cardiocytes, contrasting with most other endocrine secretory systems.
Cytosolic Ca2+ reduction may stimulate basal ANF release unlike typical endocrine cells; leaves open relevance to human cardiac regulation.
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.
No takes yet. Share an insight, caveat, or question.
Mercedes L. Kuroski de Bold (1989) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: