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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:1768.)
© 2007 American Heart Association, Inc.

Vascular Biology

Increased Inhibition of Inward Rectifier K⁺ Channels by Angiotensin II in Small-Diameter Coronary Artery of Isoproterenol-Induced Hypertrophied Model

Won Sun Park; Jae-Hong Ko; Nari Kim; Youn Kyoung Son; Sung Hyun Kang; Mohamad Warda; In Duk Jung; Yeong-Min Park; Jin Han

From the Mitochondrial Signaling Laboratory (W.S.P., J.-H.K., N.K., Y.K.S., S.H.K., M.W., J.H.), Mitochondria Research Group, Department of Physiology and Biophysics, College of Medicine, Biohealth Products Research Center, Cardiovascular and Metabolic Disease Research Center, Inje University, Busan, Korea; and the Department of Microbiology and Immunology and National Research Laboratory of Dendritic Cell Differentiation & Regulation (I.D.J., Y.-M.P.), Medical Research Institute, Pusan National University, College of Medicine, Ami-dong 1-10, Seo-gu, Busan 602-739, South Korea.

Correspondence to Jin Han, MD, PhD, Mitochondrial Signaling Laboratory, Mitochondria Research Group, Department of Physiology & Biophysics, College of Medicine, Biohealth Products Research Center, Cardiovascular and Metabolic Disease Center, Inje University 633-165 Gaegeum-Dong, Busanjin-Gu, Busan 613-735, Korea. E-mail phyhanj{at}ijnc.inje.ac.kr

Objective— We investigated the effects of angiotensin II (Ang II) on inward rectifier K⁺ (Kir) channels in small-diameter coronary arterial smooth muscle cells (SCASMCs) of control and isoproterenol (Iso)-induced hypertrophied rabbits.

Methods and Results— Kir current amplitude and Kir channel protein expression were definitely lower in the Iso-induced hypertrophied model than in the control. In a pressurized arterial experiment, 15 mmol/L K⁺-induced vasodilation was greater in the control arteries than in the arteries of Iso-induced hypertrophied model. Ang II reduced the Kir current in a concentration-dependent manner, and this inhibition was greater in SCASMCs from Iso-induced hypertrophied model than from control. Although, there was no difference in the expression of Ang II type 2 (AT₂) receptor between SCASMCs of control and Iso-induced hypertrophied model, the expression of Ang II type 1 (AT₁) receptor and phosphorylated PKC were greater in SCASMCs of Iso-induced hypertrophied model than of control.

Conclusion— Ang II inhibits Kir channels more prominently in SCASMCs of Iso-induced hypertrophied model owing to increases in the expression of AT₁ receptor and the activation of PKC. Our findings about the differential expression of Kir channels and different modulation of Kir channels by a vasoconstrictor (Ang II) in a hypertrophy model are important for better understanding the responsiveness of small-diameter arteries during hypertrophy.

Kir current amplitude was definitely lower in the coronary arterial smooth muscle cells of Iso-induced hypertrophied model than in the control. Ang II inhibits Kir current, which is more prominent in Iso-induced hypertrophied model owing to increases in the expression of AT₁ receptor and the activation of PKC. The results help for better understanding the responsiveness of small-diameter arteries during hypertrophy.

Key Words: inward rectifier K⁺ channel • hypertrophy • angiotensin II • PKC • microcirculation