SPATIAL LOCALIZATION OF AGONIST-INDUCED CA-2- DIFFERENT PATTERNS INDUCED BY HISTAMINE AND ANGIOTENSIN-II, AND RELATIONSHIP TO CATECHOLAMINERELEASE( ENTRY IN BOVINE ADRENAL CHROMAFFIN CELLS )

Citation
Tr. Cheek et al., SPATIAL LOCALIZATION OF AGONIST-INDUCED CA-2- DIFFERENT PATTERNS INDUCED BY HISTAMINE AND ANGIOTENSIN-II, AND RELATIONSHIP TO CATECHOLAMINERELEASE( ENTRY IN BOVINE ADRENAL CHROMAFFIN CELLS ), Journal of Cell Science, 105, 1993, pp. 913-921
Citations number
54
Categorie Soggetti
Cytology & Histology
Journal title
ISSN journal
00219533
Volume
105
Year of publication
1993
Part
4
Pages
913 - 921
Database
ISI
SICI code
0021-9533(1993)105:<913:SLOACD>2.0.ZU;2-Z
Abstract
The spatial organization of agonist-induced Ca2+ entry in single bovin e adrenal chromaffin cells has been investigated using video-imaging t echniques to visualize fura-2 quenching by the Ca2+ surrogate, Mn2+. T he potent secretagogue histamine, in addition to releasing Ca2+ from i ntracellular stores, resulted in a large influx of external Mn2+ that occurred over the entire surface of the cell. The influx of Ca2+ that this mirrors was found to be an obligatory requirement for the trigger ing of catecholamine release by histamine, which suggests that such a global influx of Ca2+ into the cell probably underlies the ability of this agonist to stimulate a large secretory response. By contrast, the weaker secretagogue angiotensin II, which also acts through the secon d messenger inositol trisphosphate, produced a localized entry of exte rnal Mn2+ in 64% of cells. In these cells, localized Mn2+ entry always occurred at the pole of the cell in which the angiotensin II-induced rise in [Ca2+]i was largest. Since exocytosis in response to angiotens in II has previously been shown to be restricted to this same pole of the cell (Cheek et al. (1989). J. Cell Biol. 109, 1219-1227), these re sults suggest that localized influx of Ca2+ in response to angiotensin II could underlie the polarized exocytotic response observed with thi s stimulus. These results directly demonstrate that different agonists can induce different patterns of divalent cation influx in the same c ells and, furthermore, suggest how these different patterns can have a direct influence on cellular function.