Korean J Physiol Pharmacol.  2020 Jan;24(1):111-119. 10.4196/kjpp.2020.24.1.111.

Decreased inward rectifier and voltage-gated K⁺ currents of the right septal coronary artery smooth muscle cells in pulmonary arterial hypertensive rats

  • 1Department of Physiology, Seoul National University College of Medicine, Seoul 03080, Korea. physiolksj@gmail.com
  • 2Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
  • 3Department of Nursing, Chung-Ang University, Seoul 06974, Korea. hyoo@cau.ac.kr
  • 4Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul 03080, Korea.


In vascular smooth muscle, K⁺ channels, such as voltage-gated K⁺ channels (Kv), inward-rectifier K⁺ channels (Kir), and big-conductance Ca²âº-activated K⁺ channels (BK(Ca)), establish a hyperpolarized membrane potential and counterbalance the depolarizing vasoactive stimuli. Additionally, Kir mediates endothelium-dependent hyperpolarization and the active hyperemia response in various vessels, including the coronary artery. Pulmonary arterial hypertension (PAH) induces right ventricular hypertrophy (RVH), thereby elevating the risk of ischemia and right heart failure. Here, using the whole-cell patch-clamp technique, we compared Kv and Kir current densities (I(Kv) and I(Kir)) in the left (LCSMCs), right (RCSMCs), and septal branches of coronary smooth muscle cells (SCSMCs) from control and monocrotaline (MCT)-induced PAH rats exhibiting RVH. In control rats, (1) I(Kv) was larger in RCSMCs than that in SCSMCs and LCSMCs, (2) I(Kv) inactivation occurred at more negative voltages in SCSMCs than those in RCSMCs and LCSMCs, (3) I(Kir) was smaller in SCSMCs than that in RCSMCs and LCSMCs, and (4) I(BKCa) did not differ between branches. Moreover, in PAH rats, I(Kir) and I(Kv) decreased in SCSMCs, but not in RCSMCs or LCSMCs, and I(BKCa) did not change in any of the branches. These results demonstrated that SCSMC-specific decreases in I(Kv) and I(Kir) occur in an MCT-induced PAH model, thereby offering insights into the potential pathophysiological implications of coronary blood flow regulation in right heart disease. Furthermore, the relatively smaller I(Kir) in SCSMCs suggested a less effective vasodilatory response in the septal region to the moderate increase in extracellular K⁺ concentration under increased activity of the myocardium.


Coronary artery; Inward rectifier K⁺ channel; Pulmonary arterial hypertension; Potassium channel; Smooth muscle

MeSH Terms

Coronary Vessels*
Heart Diseases
Heart Failure
Hypertrophy, Right Ventricular
Membrane Potentials
Muscle, Smooth*
Muscle, Smooth, Vascular
Myocytes, Smooth Muscle*
Patch-Clamp Techniques
Potassium Channels
Septum of Brain
Potassium Channels
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