Responses to adenosine, the A1 receptor agonist CPA, and the A2 receptor agonist CPCA were investigated in the hindlimb vascular bed of the cat under constant-flow conditions. Vasodilator responses to CPA and CPCA were reduced by the A1 recepotor antagonist C-199 (0.5 mg/kg iv) and the A2 antagonist KF15372 (1-2 mg/kg iv), respectively. Vasodilator responses to adenosine were also significantly reduced in the presence of C-199 but not KF15372, suggesting that vasodilator responses to adenosine are mediated by A1 receptors in the hindlimb vascular bed. Vasodilator responses to ATP and the nonhydrolyzable ATP analog ATPγS were not attenuated in the presence of C-199 or KF15372 or the combination of both antagonists, suggesting that vasodilator responses to ATP are not mediated by activation of adenosine type 1 or type 2 receptors. Following treatment with the nitric oxide synthase inhibitor L-NAME (100 mg/kg iv) in a dose that significantly reduced vasodilator responses to acetylcholine, and the cyclooxygenase inhibitor meclofenemate (2.5 mg/kg iv) in a dose that reduced vasodilator responses to arachidonic acid, hindlimb vasodilator responses to adenosine, CPA, CPCA, ATP and ATPγS were unaltered. In summary, these data suggest that vasodilator responses to adenosine, CPA, CPCA, ATP and ATPγS are not dependent on the activation of the cyclooxygenase pathway or release of nitric oxide. Moreover, the present data suggest that vasodilator responses to ATP are not mediated by adenosine formed from the hydrolysis of ATP.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology