Mechanism of adenosine-induced vasodilation in rat diaphragm microcirculation

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The mechanism of adenosine-induced vasodilation in rat diaphragm microcirculation was investigated using laser Doppler flowmetry. Adenosine (10-5, 3.2 x 10-5, and 10-4 M), the nonselective adenosine agonist 5'-N-ethylcarboxamido-adenosine (NECA) (10-8-10-7 M), the specific A(2A) agonist 2-p-(2-carboxyethyl)phenyl-amino-5'-N-ethyl carboxamidoadenosine (CGS-21680) (10-8-10-7 M), and the adenosine agonist with higher A1-receptor affinity, R-N6-phenylisopropyladenosine (R-PIA) (10-7, 3.2 x 10-7, and 10-6 M) elicited a similar degree of incremental increase of microcirculatory flow in a dose-dependent manner. The ATP-dependent potassium (K(ATP)) channel blocker glibenclamide (3.2 x 10-6 M) significantly attenuated the vasodilation effects of these agonists. Adenosine-induced vasodilation could be significantly attenuated by the nonselective adenosine antagonist 8-(p-sulfophenyl)-theophylline (3 x 10-5 M) or the selective A(2A) antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl ) phenol (ZM-241385, 10-6 M), but not by the selective A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (5 x 10-8 M). Adenylate cyclase inhibitor N-(cis-2-phenyl-cyclopentyl) azacyclotridecan-2-imine-hydrochloride (MDL-12330A, 10-5M) effectively suppressed the vasodilator response of adenosine and forskolin. These results suggest that adenosine-induced vasodilation in rat diaphragm microcirculation is mediated through the stimulation of A(2A) receptors, which are coupled to adenylate cyclase activation and opening of the K(ATP) channel.

Original languageEnglish
Pages (from-to)H2210-H2217
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5 48-5
Publication statusPublished - 2000

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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