Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
Published Online
on May 24, 2007

Arteriosclerosis, Thrombosis, and Vascular Biology. 2007
Published online before print May 24, 2007, doi: 10.1161/ATVBAHA.107.143339
A more recent version of this article appeared on August 1, 2007
This Article
Right arrow Full Text (PDF)
Right arrow Data Supplement
Right arrow All Versions of this Article:
27/8/1768    most recent
ATVBAHA.107.143339v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Park, W. S.
Right arrow Articles by Han, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Park, W. S.
Right arrow Articles by Han, J.

Submitted on January 12, 2007
Accepted on April 28, 2007

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 ; and 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.

* To whom correspondence should be addressed. 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{alpha} 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{alpha}. 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.
Key words: inward rectifier K+ channel • hypertrophy • angiotensin II • PKC{alpha} • microcirculation






ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.