Title : Heterogeneous mechanisms of endothelium-dependent relaxation for thrombin and peptide activators of protease-activated receptor-1 in porcine isolated coronary artery.

Pub. Date : 2000 May

PMID : 10781015






4 Functional Relationships(s)
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1 Relaxations to thrombin, SFLLRN, trypsin and SLIGRL were significantly inhibited (P<0.05) to similar extents by the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine (L-NOARG; 100 microM) and the NO scavenger oxyhaemoglobin (20 microM), both separately and in combination. Nitroarginine coagulation factor II, thrombin Homo sapiens
2 In the presence of the L-type voltage-operated calcium channel (L-VOCC) inhibitor nifedipine (0.3 microM), K(+) (67 mM) abolished the L-NOARG-resistant relaxations to thrombin, SFLLRN, trypsin and SLIGRL. Nitroarginine coagulation factor II, thrombin Homo sapiens
3 Furthermore, L-NOARG-resistant relaxations to thrombin were abolished by nifedipine, whereas relaxations to SFLLRN, trypsin or SLIGRL were not further inhibited by combined treatment with nifedipine and L-NOARG, than they were with L-NOARG treatment alone. Nitroarginine coagulation factor II, thrombin Homo sapiens
4 Similar selective inhibition of the L-NOARG-resistant relaxation to thrombin, but not SFLLRN, occurred with verapamil (1 microM) and diltiazem (3 microM). Nitroarginine coagulation factor II, thrombin Homo sapiens