Contribution of vascular tissue to the antiplatelet activity of sodium nitroprusside

We tested whether or not platelet inhibition by sodium nitroprusside (SNP) was enhanced by vascular tissue production of nitric oxide (NO) and calcitonin gene-related peptide (CGRP) release. Platelet aggregation was determined with whole blood impedance aggregometry after incubations of SNP in the presence or absence of rat aortic tissue (AT) or AT + CGRPS(8-37) (a specific CGRP antagonist). SNP alone had no effect on platelet aggregation until 100 mu M was used (2.3 + 1.5 Omega vs, control aggregation of 9.9 + 2.0 Omega; p < 0.001). Go-incubation of AT with SNP significantly enhanced platelet inhibition at 1 (1.6 +/- 1.3 Omega; p < 0.001), 10 (0.7 +/- 0.4 Omega; p < 0.001), and 100 mu M (0.3 +/- 0.3 Omega; p < 0.001). CGRP(8-37) did not significantly antagonize aggregation by SNP + AT (p > 0.05). The inhibition of platelet aggregation by 10 mu M SNP was inhibited by methylene blue (MB) (9.0 +/- 1.7 Omega at 10 mu M; 11.7 +/- 2.4 Omega at 100 mu M; p < 0.001) but not by 30 mu M L-N-theta-monomethyl-L-arginine (L-NMMA; 2.9 +/- 1.8 Omega; p > 0.05). These results indicate that vascular tissue significantly contributes to the ability of SNP to inhibit platelet aggregation probably through greater vascular enzymatic production of NO, but not by releasing CORP in contrast to nitroglycerin.