Lowering of Blood Pressure Improves Endothelial Dysfunction by Increase of Nitric Oxide Production in Hypertensive Rats.

DOI PubMed 被引用文献14件 参考文献58件
  • HATTA Tsuguru
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • NAKATA Tetsuo
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • HARADA Sanae
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • KIYAMA Masahiro
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • MORIGUCHI Jiro
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • MORIMOTO Satoshi
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • ITOH Hiroshi
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • SASAKI Susumu
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • TAKEDA Kazuo
    Second Department of Medicine, Kyoto Prefectural University of Medicine
  • NAKAGAWA Masao
    Second Department of Medicine, Kyoto Prefectural University of Medicine

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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. (Hypertens Res 2002; 25: 455-460)

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