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Departments of 1 Pharmacology and 2 Internal Medicine, College of Medicine, Pusan National University, Pusan 602-739; and 3 Center for Biofunctional Molecules, Pohang University of Science and Technology, Pohang 790-600, Korea
This study was aimed to investigate the
underlying mechanism of vasodilation induced by the activation of
A2B adenosine receptors in relation to cerebral blood flow
(CBF) autoregulation. Changes in pial arterial diameters were observed
directly through a closed cranial window.
N
-nitro-L-arginine methyl ester
(L-NAME, nitric oxide synthase inhibitor) significantly
suppressed the concentration-dependent vasodilations induced by
adenosine and 5'-N-ethylcarboxamido-adenosine (NECA) but
not the vasodilation by CGS-21680 (A2A-receptor agonist). Moreover, NECA-induced vasodilation was suppressed by alloxazine (1 µmol/l) but not by ZM-241385 (1 µmol/l, A2A
antagonist), which suggests mediation by A2B- receptor
activation. Otherwise, the level of nitrite/nitrate was concentration
dependently increased in the artificial cerebrospinal fluid (CSF) when
adenosine and NECA were suffused over the cortical surface.
L-NAME and alloxazine, but not ZM-241385, largely inhibited
their releases. The lower limit of CBF autoregulation was little
affected following pretreatment with L-NAME or alloxazine.
Thus it is suggested that adenosine-induced vasodilation via activation
of A2B-adenosine receptors of the rat pial artery is
coupled to the production of nitric oxide, which contributes little to
CBF autoregulation.
5'-N-ethylcarboxamido-adenosine; N-nitro-L-arginine methyl ester; alloxazine; nitrite/nitrate
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