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The role of ATP-sensitive potassium channels in regulating coronary microcirculation
T Komaru1, H Kanatsuka, K Dellsperger
1First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Insights
The ATP-sensitive potassium channel (K+ATP channel) is crucial for coronary arteriolar function during autoregulation and reactive hyperemia. However, it does not significantly influence acetylcholine-induced vasodilation in these vessels.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Ion Channel Function
Background:
- ATP-sensitive potassium channels (K+ATP channels) are present in blood vessels and influence vascular tone.
- Their specific role in coronary microvascular responses requires detailed investigation.
Purpose of the Study:
- To investigate the role of K+ATP channels in coronary arteriolar vasomotion.
- To examine their involvement in coronary autoregulation, ischemia, reactive hyperemia, and acetylcholine-induced responses in vivo.
Main Methods:
- Experiments were conducted on anesthetized open-chest dogs.
- Coronary arterioles were directly observed in situ using specialized optical systems.
- Pharmacological blockade of K+ATP channels was achieved using glibenclamide.
Main Results:
- K+ATP channels mediated vasodilation during reduced perfusion pressure and reactive hyperemia.
- Glibenclamide significantly inhibited these K+ATP channel-dependent dilations.
- Acetylcholine-induced vasodilation was not affected by glibenclamide, suggesting a K+ATP channel-independent mechanism.
Conclusions:
- K+ATP channels are vital for coronary microvascular vasomotion during autoregulation, ischemia, and reactive hyperemia.
- These channels do not appear to play a significant role in endothelium-dependent vasodilation mediated by acetylcholine in coronary arterioles in vivo.
Abstract:
The ATP-sensitive potassium channel (K+ATP channel) is known to exist in blood vessels and to regulate vascular tone. We examined the role of this channel in coronary arteriolar vasomotion during coronary autoregulation, ischemia, reactive hyperemia and endothelium-dependent response by acetylcholine in vivo. Experiments were performed with anesthetized open-chest dogs. Coronary arterioles were directly observed in situ by means of a floating objective system or a stroboscopic epi-illumination system synchronized with cardiac motion. Small arterioles less than 100 microns in internal diameter dilated in response to reduction in perfusion pressure (perfusion pressure: 60, 40, 25 mm Hg). Glibenclamide, a selective blocker of the K+ATP channel, reversed the dilation. Reactive hyperemia produced by 20-second occlusion of the left anterior descending coronary artery resulted in arteriolar dilation, the magnitude of which was greater in smaller arterioles than in larger ones. Glibenclamide significantly inhibited the dilation in both large and small arterioles. Acetylcholine (ACh) produced dilation in arterioles of all sizes. NG-monomethyl L-arginine, a competitive inhibitor of nitric oxide synthesis, abolished the dilation of large arterioles, but failed to abolish the dilation in small arterioles. Glibenclamide, however, did not have any additional inhibitory effect on ACh-induced arteriolar dilation. Thus, we conclude that the K+ATP channel plays an important role in coronary microvascular vasomotion during autoregulation, ischemia and reactive hyperemia, but not during endothelium-dependent vasodilation induced by ACh in vivo.