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Uehara Y, Fujimi K, Yahiro E, Abe S, Devarajan S, Saku K, Urata H. Induction of tissue angiotensin II-forming activity in two-kidney, one-clip hypertensive hamster model. World J Hypertens 2013; 3(2): 9-17 [DOI: 10.5494/wjh.v3.i2.9]
Yoshinari Uehara, Kanta Fujimi, Eiji Yahiro, Satomi Abe, Keijiro Saku, Department of Cardiology, Fukuoka University School of Medicine, Fukuoka 814-0180, Japan
Sankar Devarajan, Hidenori Urata, Department of Cardiovascular Diseases, Fukuoka University Chikushi Hospital, Chikushino 818-8502, Japan
Author contributions: All authors contributed to this work. Uehara Y, Fujimi K and Yahiro E contributed equally to this work.
Correspondence to: Yoshinari Uehara, MD, PhD, Department of Cardiology, Fukuoka University School of Medicine, 7-45-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. ueharay@fukuoka-u.ac.jp
Telephone: +81-92-8011011 Fax: +81-92-8652692
Received: April 19, 2013 Revised: May 9, 2013 Accepted: May 20, 2013 Published online: May 23, 2013 Processing time: 86 Days and 16 Hours
Core Tip
Core tip: There are several pathways that can produce angiotensin (Ang) II in human tissues, which are involved in remodeling of the cardiovascular system. Among these, chymase has been exhibited the greatest Ang II-forming enzyme in human heart. In hypertensive hamster, blood pressure was significantly elevated, and both Ang converting enzyme (ACE) inhibitor (ACE-I) and Ang II type 1 receptor antagonist (ARB) revealed similar antihypertensive effects. Interestingly, cardiac chymase-dependent Ang II-formation decreased after ACE-I or ARB treatment. In addition, chymase-dependent Ang II-formation increased in the aorta, although these changes were inhibited only by ARB. ACE and chymase were regulated in a tissue-dependent manner in hypertensive hamsters, and the both enzymes were independently regulated.
