Abstract
We investigated the effect of black currant (BC) concentrate on smooth muscle in rat thoracic aorta. BC concentrate dose-dependently relaxed the norepinephrine (0.1 μM)-precontracted aorta, and the response was abolished after endothelium removal. Both oxyhemoglobin (1 μM), a nitric oxide (NO) scavenger, and 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ, 0.5 μM), an inhibitor of guanylyl cyclase (GC), inhibited the relaxing effect of BC concentrate. NG-nitro-L-arginine methyl ester (L-NAME, 10 μM), a nitric oxide synthase (NOS) inhibitor, inhibited the relaxation, and the subsequent addition of L-arginine (1 mM), a NOS substrate, reversed the inhibitory effects of L-NAME. Neither indomethacin (10 μM), an inhibitor of cyclooxygenase, nor atropine (1 μM), an antagonist of muscarinic receptors, modified the effect of BC concentrate. Diphenhydramine (3 μM) and chlorpheniramine (2 μM), selective antagonists of H1-receptors, inhibited the relaxation, but cimetidine (0.3 mM), a selective antagonist of H2-receptors, did not affect the relaxation. These results indicate that, in the rat aorta, BC concentrate enhances synthesis of NO, which subsequently induces the endothelium-dependent vasorelaxation via the H1-receptors on the endothelium.
