モリモト　サトシ   Morimoto Satoshi   森本　聡    所属   医学部 医学科（東京女子医科大学病院）    職種   准教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Lowering of blood pressure improves endothelial dysfunction by increase of nitric oxide production in hypertensive rats.
掲載誌名	正式名：Hypertension research : official journal of the Japanese Society of Hypertension 略　 称：Hypertens Res ISSNコード：09169636/09169636
掲載区分	国外
巻・号・頁	25(3),pp.455-60
著者・共著者	Hatta Tsuguru, Nakata Tetsuo, Harada Sanae, Kiyama Masahiro, Moriguchi Jiro, Morimoto Satoshi, Itoh Hiroshi, Sasaki Susumu, Takeda Kazuo, Nakagawa Masao
発行年月	2002/05
概要	To investigate the effects of angiotensin converting enzyme inhibitor (ACE-I) and other antihypertensive agents on the nitric oxide (NO) release during hypertension, seven- and fourteen-week-old SHR and deoxycorticosterone acetate (DOCA)-salt rats were treated with hydralazine, manidipine (Ca antagonist) or quinapril (ACE-I) for 3 weeks to lower blood pressure. Systolic blood pressure (SBP) was measured by the tail cuff method once each week. Endothelial cells (ECs) derived from the descending aorta of the treated rats were cultured and NOx levels in culture media were measured with an NO analyzer based on the Griess reaction. In both SHR and DOCA-salt rats, antihypertensive therapy lowered SBP to levels similar to those of control rats. The only exception was quinapril treatment of DOCA-salt rats. Although NOx release by ECs derived from hypertensive rats was improved by antihypertensive therapy, the effect was most pronounced in SHR treated with quinapril. In addition, restoration of NOx release was much more remarkable in younger SHR. NOx release was significantly higher in DOCA-salt rats treated with quinapril than in control rats without reduction of SBP. These results suggest that lowering blood pressure improves release of NO by ECs during hypertension and that the time at which antihypertensive therapy is started is also important to preserve endothelial function. Furthermore, ACE-I is suggested to protect endothelial function by increasing NO production in addition to lowering blood pressure.
DOI	10.1291/hypres.25.455
PMID	12135326