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This likely occurred as the particular modulatory effects on the nitric oxide (NO)-system as a whole, induced NO-release on its own [61,62,63], counteracted NO-synthase (NOS)-inhibition [61] (i.e., N(G)-nitro-L-arginine methylester (L-NAME)-hypertension and pro-thrombotic effect) [58,62], and counteracted NO-over-stimulation [61] (L-arginine-hypotension and anti-thrombotic, pro-bleeding effect) [58,62]
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