Tags

Type your tag names separated by a space and hit enter

Increased inward rectifier K+ current of coronary artery smooth muscle cells in spontaneously hypertensive rats; partial compensation of the attenuated endothelium-dependent relaxation via Ca2+ -activated K+ channels.
Clin Exp Pharmacol Physiol. 2020 01; 47(1):38-48.CE

Abstract

Endothelium-dependent vasorelaxation is partly mediated by small-conductance (SK3) and intermediate-conductance Ca2+ -activated K+ channels (SK4) in the endothelium that results in endothelium-dependent hyperpolarization (EDH). Apart from the electrical propagation through myoendothelial gap junctions, the K+ released from the endothelium facilitates EDH by increasing inward rectifier K+ channel (Kir) conductance in smooth muscle cells. The EDH-dependent relaxation of coronary artery (CA) and Kir current in smooth muscle cells (CASMCs) of hypertensive animals are poorly understood despite the critical role of coronary flow in the hypertrophic heart. In spontaneously hypertensive (SHR) and control (WKY) rats, we found attenuation of the CA relaxation by activators of SK3 and SK4 (NS309 and 1-EBIO) in SHR. In isolated CASMCs, whole-cell patch-clamp study revealed larger IKir in SHR than WKY, whereas the myocytes of skeletal and cerebral arteries showed smaller IKir in SHR than WKY. While the treatment with IKir inhibitor (0.1 mmol/L Ba2+) alone did not affect the WKY-CA, the SHR-CA showed significant contractile response, suggesting relaxing influence of the higher IKir in the CASMCs of SHR. Furthermore, the attenuation of NS309-induced relaxation of CA by the combined treatment with 0.1 mmol/L Ba2+ was more prominent in SHR than WKY. Our study firstly shows a distinct increase of IKir in the CASMCs of SHR, which could partly compensate for the attenuated relaxation via endothelial SK3 and SK4.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Kim HJ
Department of Physiology, Seoul National University College of Medicine, Seoul, Korea. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
Yin MZ
Department of Physiology, Seoul National University College of Medicine, Seoul, Korea. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
Cho S
Department of Physiology, Seoul National University College of Medicine, Seoul, Korea. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
Kim SE
Department of Physiology, Seoul National University College of Medicine, Seoul, Korea. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
Choi SW
Department of Physiology, Seoul National University College of Medicine, Seoul, Korea. Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, Korea.
Ye SK
Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea. Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, Korea. Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea.
Yoo HY
Chung-Ang University Red Cross College of Nursing, Seoul, Korea.
Kim SJ
Department of Physiology, Seoul National University College of Medicine, Seoul, Korea. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea. Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, Korea.

MeSH

AcetylcholineAnimalsCoronary VesselsEndothelium, VascularHypertensionMembrane PotentialsMesenteric ArteriesMuscle ContractionMuscle, Smooth, VascularMyocytes, Smooth MusclePotassium Channels, Calcium-ActivatedPotassium Channels, Inwardly RectifyingRatsRats, Inbred SHRRats, Inbred WKYVasodilation

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

31444788

Citation

Kim, Hae Jin, et al. "Increased Inward Rectifier K+ Current of Coronary Artery Smooth Muscle Cells in Spontaneously Hypertensive Rats; Partial Compensation of the Attenuated Endothelium-dependent Relaxation Via Ca2+ -activated K+ Channels." Clinical and Experimental Pharmacology & Physiology, vol. 47, no. 1, 2020, pp. 38-48.
Kim HJ, Yin MZ, Cho S, et al. Increased inward rectifier K+ current of coronary artery smooth muscle cells in spontaneously hypertensive rats; partial compensation of the attenuated endothelium-dependent relaxation via Ca2+ -activated K+ channels. Clin Exp Pharmacol Physiol. 2020;47(1):38-48.
Kim, H. J., Yin, M. Z., Cho, S., Kim, S. E., Choi, S. W., Ye, S. K., Yoo, H. Y., & Kim, S. J. (2020). Increased inward rectifier K+ current of coronary artery smooth muscle cells in spontaneously hypertensive rats; partial compensation of the attenuated endothelium-dependent relaxation via Ca2+ -activated K+ channels. Clinical and Experimental Pharmacology & Physiology, 47(1), 38-48. https://doi.org/10.1111/1440-1681.13168
Kim HJ, et al. Increased Inward Rectifier K+ Current of Coronary Artery Smooth Muscle Cells in Spontaneously Hypertensive Rats; Partial Compensation of the Attenuated Endothelium-dependent Relaxation Via Ca2+ -activated K+ Channels. Clin Exp Pharmacol Physiol. 2020;47(1):38-48. PubMed PMID: 31444788.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased inward rectifier K+ current of coronary artery smooth muscle cells in spontaneously hypertensive rats; partial compensation of the attenuated endothelium-dependent relaxation via Ca2+ -activated K+ channels. AU - Kim,Hae Jin, AU - Yin,Ming Zhe, AU - Cho,Suhan, AU - Kim,Sung Eun, AU - Choi,Seong Woo, AU - Ye,Sang Kyu, AU - Yoo,Hae Young, AU - Kim,Sung Joon, Y1 - 2019/08/24/ PY - 2019/06/13/received PY - 2019/08/06/revised PY - 2019/08/19/accepted PY - 2019/8/25/pubmed PY - 2021/5/4/medline PY - 2019/8/25/entrez KW - K+ channel KW - coronary artery KW - endothelium KW - hypertension KW - inward rectifier K+ channel KW - smooth muscle SP - 38 EP - 48 JF - Clinical and experimental pharmacology & physiology JO - Clin Exp Pharmacol Physiol VL - 47 IS - 1 N2 - Endothelium-dependent vasorelaxation is partly mediated by small-conductance (SK3) and intermediate-conductance Ca2+ -activated K+ channels (SK4) in the endothelium that results in endothelium-dependent hyperpolarization (EDH). Apart from the electrical propagation through myoendothelial gap junctions, the K+ released from the endothelium facilitates EDH by increasing inward rectifier K+ channel (Kir) conductance in smooth muscle cells. The EDH-dependent relaxation of coronary artery (CA) and Kir current in smooth muscle cells (CASMCs) of hypertensive animals are poorly understood despite the critical role of coronary flow in the hypertrophic heart. In spontaneously hypertensive (SHR) and control (WKY) rats, we found attenuation of the CA relaxation by activators of SK3 and SK4 (NS309 and 1-EBIO) in SHR. In isolated CASMCs, whole-cell patch-clamp study revealed larger IKir in SHR than WKY, whereas the myocytes of skeletal and cerebral arteries showed smaller IKir in SHR than WKY. While the treatment with IKir inhibitor (0.1 mmol/L Ba2+) alone did not affect the WKY-CA, the SHR-CA showed significant contractile response, suggesting relaxing influence of the higher IKir in the CASMCs of SHR. Furthermore, the attenuation of NS309-induced relaxation of CA by the combined treatment with 0.1 mmol/L Ba2+ was more prominent in SHR than WKY. Our study firstly shows a distinct increase of IKir in the CASMCs of SHR, which could partly compensate for the attenuated relaxation via endothelial SK3 and SK4. SN - 1440-1681 UR - https://www.unboundmedicine.com/medline/citation/31444788/Increased_inward_rectifier_K+_current_of_coronary_artery_smooth_muscle_cells_in_spontaneously_hypertensive_rats DB - PRIME DP - Unbound Medicine ER -