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Selected Publication:
Graier, WF; Holzmann, S; Hoebel, BG; Kukovetz, WR; Kostner, GM.
Mechanisms of L-NG nitroarginine/indomethacin-resistant relaxation in bovine and porcine coronary arteries.
Br J Pharmacol. 1996; 119(6):1177-1186
Doi: 10.1111/j.1476-5381.1996.tb16020.x
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- Leading authors Med Uni Graz
- Graier Wolfgang
- Co-authors Med Uni Graz
- Kostner Gerhard
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- Abstract:
- 1. Coronary arteries from bovines (BCA) and pigs (PCA) were used for measuring endothelium-dependent relaxation in the presence of L-NG nitroarginine and indomethacin. As some compounds tested have been found to have an inhibitory effect on autacoid-activated endothelial Ca2+ signalling, endothelium-dependent relaxation was initiated with the Ca2+ ionophore A23187. 2. The common compounds for modulating arachidonic acid release/pathway, mepacrine and econazole only inhibited L-NG nitroarginine-resistant relaxation in BCA not in PCA. In contrast, proadifen (SKF 525A) diminished relaxation in BCA and PCA. Mepacrine and proadifen inhibited Hoe-234-initiated relaxation in BCA and PCA, while econazole only inhibited Hoe 234-induced relaxation in PCA. Due to the multiple effects of these compounds, caution is necessary in the interpretation of results obtained with these compounds. 3. The inhibitor of Ca(2+)-activated K+ channels, apamin, strongly attenuated A23187-induced L-NG nitroarginine-resistant relaxation in BCA while apamin did not affect L-NG nitroarginine-resistant relaxation in PCA. 4. Pertussis toxin blunted L-NG nitroarginine-resistant relaxation in BCA, while relaxation of PCA was not affected by pertussis toxin. 5. Thiopentone sodium inhibited endothelial cytochrome P450 epoxygenase (EPO) in PCA but not in BCA, while L-NG nitroarginine-resistant relaxation of BCA and PCA were unchanged. Protoporphyrine IX inhibited EPO in BCA and PCA and abolished L-NG nitroarginine-resistant relaxation of BCA not PCA. 6. An EPO-derived compound, 11,12-epoxy-eicosatrienoic acid (11,12-EET) yielded significant relaxation in BCA and PCA in three out of six experiments. 7. These findings suggest that L-NG nitroarginine-resistant relaxation in BCA and PCA constitutes two distinct pathways. In BCA, activation of Ca(2+)-activated K+ channels via a pertussis-toxin-sensitive G protein and EPO-derived compounds might be involved. In PCA, no selective inhibition of L-NG nitroarginine-resistant relaxation was found.
- Find related publications in this database (using NLM MeSH Indexing)
- 8,11,14-Eicosatrienoic Acid - analogs and derivatives
- Animals - analogs and derivatives
- Apamin - pharmacology
- Calcimycin - pharmacology
- Cattle - pharmacology
- Coronary Vessels - drug effects
- Cytochrome P-450 Enzyme System - physiology
- Indomethacin - pharmacology
- Nitroarginine - pharmacology
- Ouabain - pharmacology
- Pertussis Toxin - pharmacology
- Potassium Channels - drug effects
- Protoporphyrins - pharmacology
- Swine - pharmacology
- Thiopental - pharmacology
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- Find related publications in this database (Keywords)
- G Protein
- Bradykinin
- A23187
- Endothelium-Derived Relaxing Factor
- Ouabain
- Thiopentone Sodium
- Protoporphyrine Tx