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Potassium channels sensitive to combination of charybdotoxin and apamin regulate the tone of diabetic isolated canine coronary arteries
Author(s) -
Pataricza J.,
Márton Z.,
Lengyel Cs.,
Tóth M.,
Papp J. Gy.,
Varró A.,
Kun A.
Publication year - 2008
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2008.01859.x
Subject(s) - charybdotoxin , apamin , medicine , calcium activated potassium channel , potassium channel , endocrinology , vasodilation , coronary arteries , artery , chemistry , acetylcholine , cardiology
Aims: Functional roles of calcium‐activated potassium channels on the mechanical activity of epicardial coronary arteries obtained from a canine model of diabetes were investigated. Methods: Coronary arteries were isolated from healthy, alloxan‐diabetic and insulin‐treated diabetic dogs. Basal tensions, contractions induced by the prostaglandin (PG) analogue, U46619, and endothelium‐dependent relaxations to acetylcholine (ACh) were modified with charybdotoxin (CHTX) + apamin (APA), inhibitors of calcium‐activated potassium channels, as well as with N ω ‐nitro‐ l ‐arginine (LNA) + indomethacin (INDO) to suppress the synthesis of nitric oxide (NO) and PGs. The relaxing effect of nitroprusside‐sodium (SNP), an NO donor, was also determined. Results: In diabetic coronary arteries, CHTX + APA did not change while LNA + INDO elevated the basal tension. PG‐induced contractions were enhanced by CHTX + APA and by LNA + INDO in all the three groups of animals. CHTX + APA decreased the maximal relaxations to ACh in a partly insulin‐dependent manner. LNA + INDO abolished the endothelium‐dependent relaxations to ACh. In diabetic coronary arteries, the sensitivity to SNP‐induced relaxation was enhanced, insulin independently, suggesting that NO could be partly responsible for maintaining intact ACh‐induced vasorelaxation. Conclusion: In diabetic canine coronary artery, the vasomotor responses reflect up‐regulation of calcium‐activated potassium channels. This endothelial mechanism of the canine epicardial coronary artery may oppose vasoconstrictions in diabetic vascular tissue.