Fig. 2.

Mechanism of P2Y₁-mediated coronary arteriolar dilation. A: ADP analog 2-methylthio-ADP (2-MeS-ADP) produced dose-dependent vasodilation under control conditions. This vasodilation was abolished by the P2Y₁ antagonist MRS-2179 (10 μM) or the nitric oxide synthase inhibitor N^G-nitro-l-arginine methyl ester (l-NAME, 300 μM). B: ATP produced dose-dependent vasodilation under control conditions that was attenuated by MRS-2179. C: nonhydrolyzable ATP analog ATPγS produced dose-dependent vasodilation under control conditions that was rightward shifted by MRS-2179. Values are means ± SE of number of samples in parentheses. Where error bars are not shown, they are within the symbol. *P < 0.05 vs. MRS-2179. **P < 0.05 vs. all other groups.