Animal study demonstrates that blocking ATP-sensitive potassium channels impairs parathyroid hormone-mediated coronary dilation in dogs, indicating a key role in vascular regulation.
Objective: The aim of the present study was to characterize the role of the ATP-sensitive potassium channels (K⁺ATP) in the coronary dilator action of parathyroid hormone (PTH). Methods: Dose-response curves of intracoronary administrated PTH (0.15–1.33 nmol) were obtained in control phases and during continuous intracoronary administration of the K⁺ATP channel-selective antagonist glibenclamide (0.1–1.0 µmol/min) in dogs (n = 13). Results: Increments of integrated coronary conductance (excess coronary conductance) at PTH doses of 0.15 and 1.33 nmol were 1.17 versus 0.03 ml/mm Hg (p < 0.05) and 4.03 versus 0.94 ml/mm Hg (p < 0.05) in the control versus during maximal blockade, respectively. Conclusion: The results indicate that the activation of K⁺ATP channels significantly contributes to the PTH-induced coronary vasodilation.
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