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Angiotensin II Effects on the Cytosolic Free Ca 2+ Concentration in N1E‐115 Neuroblastoma Cells: Kinetic Properties of the Ca 2+ Transient Measured in Single Fura‐2‐Loaded Cells
Author(s) -
Monck Jonathan R.,
Williamson Robert E.,
Rogulja Ivo,
Fluharty Steven J.,
Williamson John R.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb13312.x
Subject(s) - angiotensin ii , pertussis toxin , endocrinology , chemistry , medicine , phospholipase c , fura 2 , bradykinin , cytosol , biophysics , inositol , receptor , g protein , biochemistry , biology , enzyme
The effect of angiotensin II on the cytosolic free Ca 2+ concentration was measured in single mouse neuroblastoma N1E‐115 cells loaded with fura‐2. Angiotensin II induced a transient concentration‐dependent increase in Ca 2+ and also increased the production of inositol polyphosphates. The Ca 2+ increase did not require extracellular Ca 2+ and was unaffected by pretreatment with pertussis toxin. These data suggest that angiotensin II increased Ca 2+ by an inositol tris‐phosphate‐mediated release of intracellular Ca 2+ following activation of phospholipase C via a pertussis toxin‐insensitive guanine nucleotide binding protein. Similar results were obtained with bradykinin. The angiotensin II‐ or bradykinin‐induced increase in Ca 2+ occurred after a concentration‐dependent latent period. Low concentrations of agonist elicited a small increase in Ca 2+ following a variable lag that sometimes exceeded 1 min, whereas at maximally effective angiotensin II concentrations a larger, more rapid increase in Ca 2+ occurred without a measurable delay. In some cells, oscillatory increases in Ca 2+ were induced by angiotensin II and bradykinin. Possible mechanisms to explain the concentration dependency of the latent period and the oscillatory nature of the increases of Ca 2+ are discussed. These results indicate that the mouse neuroblastoma N1E‐115 cell represents a useful model for studying the signal response transduction mechanisms regulating the effects of angiotensin II in neuronal cells.