Article date: October 1994
By: Pierre Pacaud, Guillaume Grëgoire, Gervaise Loirand, in Volume 113, Issue 2, pages 457-462
The action of adenosine 5′‐triphosphate (ATP, lO μm) was studied in single patch‐clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai was estimated by the emission from the dye indo‐1.
In the presence of 20 μm gallopamil (D600), a blocker of voltage‐dependent Ca2+ channels, ATP applied to cells held at a holding potential of − 60 mV evoked a transient inward current and an increase in Cai.
The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed.
ATP‐induced responses were not modified by the addition of the inositol 1,4,5‐trisphosphate receptor antagonist, heparin (1 μm) in the pipette solution.
In the presence of caffeine (5 μm) or ryanodine (100 μm) in the pipette solution, which deplete the intracellular Ca2+ store, the ATP‐induced Cai rise was greatly reduced.
Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from intracellular stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP‐gated channels.
The action of adenosine 5′‐triphosphate (ATP, lO μm) was studied in single patch‐clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai was estimated by the emission from the dye indo‐1.
In the presence of 20 μm gallopamil (D600), a blocker of voltage‐dependent Ca2+ channels, ATP applied to cells held at a holding potential of − 60 mV evoked a transient inward current and an increase in Cai.
The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed.
ATP‐induced responses were not modified by the addition of the inositol 1,4,5‐trisphosphate receptor antagonist, heparin (1 μm) in the pipette solution.
In the presence of caffeine (5 μm) or ryanodine (100 μm) in the pipette solution, which deplete the intracellular Ca2+ store, the ATP‐induced Cai rise was greatly reduced.
Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from intracellular stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP‐gated channels.
DOI: 10.1111/j.1476-5381.1994.tb17011.x
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