Biology Reference
In-Depth Information
Fig. 12.6
Effects of 60 s
pulses of 10
M ATP, ADP,
UTP and acetylcholine (ACh)
on [Ca
2+
]
i
in islet endothelial
cells and
μ
-cells superfused
with a medium containing
20 mM glucose, 20 nM
glucagon and 50
β
M
methoxyverapamil. The
endothelial cells respond with
extended rises of [Ca
2+
]
i
to
ATP and UTP, but not to ADP
or acetylcholine. Spontaneous
transients are seen in
μ
-cells,
but not in endothelial cells.
Transients were promptly
elicited in
β
-cells by ATP and
ADP. Representative for 5 (
a
)
and4(
b
) experiments. From
[37]
β
β
-cells to external ATP or ADP results in
disappearance of the [Ca
2+
]
i
transients, which coordinate the hormone pulses [28].
Administered as 60-s pulses it was found that ADP temporarily suppressed glucose-
induced transients of [Ca
2+
]
i
(Fig. 12.6). Since the islet endothelial cells respond to
P2Y receptor activation with extended increase of [Ca
2+
]
i
, it is likely that the accom-
panying ATP release is prolonged. Accordingly, islet endothelial cells may have
a tonic inhibitory action on the
-cells [29, 32]. Prolonged exposure of
β
-cell transients of [Ca
2+
]
i
, resulting in impaired
synchronization of the insulin release pulses.
β
12.5 Conclusion
The pancreatic islets constitute a unique micro-organ, where both microvascular
endothelium and the endocrine cells can release and react upon ATP. A crucial
question is whether ATP released from the
β
-cells has regulatory effects on islet
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