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Comparative analysis of vasodilating Mechanisms of Kil769, Ki3315 and KRN2391, pyridinecarboximidamide derivatives, in porcine isolated coronary artery

Authors
Journal
General Pharmacology The Vascular System
0306-3623
Publisher
Elsevier
Publication Date
Volume
25
Issue
5
Identifiers
DOI: 10.1016/0306-3623(94)90100-7

Abstract

Abstract 1. The vasodilating mechanisms of pyridinecarboximidamide derivatives which have a nitroxyl group (KRN2391), a phenyl group (Ki1769) or a hydroxyl group (Ki3315) were studied in porcine isolated coronary artery. 2. KRN2391 (10 −6 M) increased cyclic GMP formation but did not affect intracellular cyclic AMP level. Ki1769 (10 −5 M) and Ki3315 (10 −3 M) had no effect on intracellular cyclic GMP and cyclic AMP levels. 3. Despite producing submaximal relaxation at KRN2391 (10 −6 M) and nitroglycerin (10 −6 M), the increase in cyclic GMP caused by KRN2391 was lower than that caused by nitroglycerin. 4. Methylene blue (10 −5 M) inhibited KRN2391- and nitroglycerin-induced relaxations but did not affect Ki1769- and Ki3315-induced relaxation. 5. Glibenclamide (10 −6 M) inhibited KRN2391-, Ki1769- and Ki3315-induced relaxation but did not affect nitroglycerin-induced relaxation. 6. These results suggest that the nitroxyl group of KRN239 contributes to its nitrate action and the pyridinecarboximidamide moiety plays an important role of developing a K channel opening action.

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