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Department of Diagnostic Radiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff CF14 4XN, United Kingdom
We have compared the mechanisms that
contribute to endothelium-derived hyperpolarizing factor (EDHF)-type
responses induced by ACh and the Ca2+ ionophore A-23187 in
the rabbit iliac artery. Relaxations to both agents were associated
with ~1.5-fold elevations in smooth muscle cAMP levels and were
attenuated by the adenylyl cyclase inhibitor 2',5'-dideoxyadenosine
(DDA) and potentiated by the cAMP phosphodiesterase inhibitor
3-isobutyl-1-methylxanthine (IBMX). Mechanical responses were inhibited
by coadministration of the Ca2+-activated K+
channel blockers apamin and charybdotoxin, both in the absence and
presence of IBMX, but were unaffected by blockade of ATP-sensitive K+ channels with the sulphonylurea glibenclamide.
Relaxations and elevations in cAMP evoked by ACh were abolished by
18
-glycyrrhetinic acid, which disrupts gap junction plaques, whereas
the corresponding responses to A-23187 were unaffected by this agent.
Consistently, in "sandwich" bioassay experiments, A-23187, but not
ACh, elicited extracellular release of a factor that evoked relaxations
that were inhibited by DDA and potentiated by IBMX. These findings provide evidence that EDHF-type relaxations of rabbit iliac arteries evoked by ACh and A-23187 depend on cAMP accumulation in smooth muscle,
but involve signaling via myoendothelial gap junctions and the
extracellular space, respectively.
connexin; cGMP; acetylcholine; A-23187
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