Key result
Glibenclamide reversed coronary arteriolar dilation during autoregulation and reactive hyperemia in dogs, demonstrating K+ATP channels regulate these processes but not ACh-induced vasodilation.
Why the study?
Does the K+ATP channel regulate coronary microvascular vasomotion during autoregulation, ischemia, reactive hyperemia, and endothelium-dependent vasodilation in vivo?
Population
Anesthetized open-chest dogs
Comparison
Glibenclamide, Acetylcholine, and NG-monomethyl… vs Baseline conditions or responses prior to blockade
Design
Preclinical
Authors
Loading...
K+ATP channels mediate canine coronary autoregulation and hyperemia; leaves open human microvascular relevance and therapeutic targeting.
Does the K+ATP channel regulate coronary microvascular vasomotion during autoregulation, ischemia, reactive hyperemia, and endothelium-dependent vasodilation in vivo?
The K+ATP channel plays a critical role in coronary microvascular vasomotion during autoregulation, ischemia, and reactive hyperemia, but not during endothelium-dependent vasodilation.
Komaru et al. (1993) studied this question. Glibenclamide was evaluated on Coronary arteriolar vasomotion during autoregulation, ischemia, reactive hyperemia and endothelium-dependent response. Glibenclamide reversed coronary arteriolar dilation during autoregulation and reactive hyperemia in dogs, demonstrating K+ATP channels regulate these processes but not ACh-induced vasodilation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: