Mechanism of Hypertension Induced by Chronic Inhibition of Nitric Oxide in Rats.

• Takahashi Hakuo

  Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University

• Hara Katsuko

  Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University

• Komiyama Yutaka

  Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University

• Masuda Midori

  Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University

• Murakami Takashi

  Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University

• Nishimura Masato

  Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine

• Nambu Akira

  Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine

• Yoshimura Manabu

  Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine

抄録

In order to clarify the mechanism of hypertension induced by a nitric oxide (NO) synthase inhibitor, L-N^G-nitro-L-arginine (LNNA), metabolites of NO, catecholamines, and hemodynamic parameters were measured during 7 days of oral administration of LNNA in rats. Control rats received either L-arginine (L-Arg) or the vehicle. Systolic blood pressure, measured by the tail-cuff method was elevated throughout the period of LNNA administration, but that in the two control groups was not influenced by treatment. Heart rate decreased on the second day only in LNNA-treated rats. Although L-Arg treatment had no influence, LNNA markedly decreased the plasma level and the urinary excretion of nitrate ions (NO₃^-). Urinary excretion of noradrenaline was significantly decreased on the second day of LNNA administration and returned to the control level thereafter. When hemodynamic changes were measured by using radioactive microspheres, LNNA was found to increase blood pressure by markedly increasing total peripheral resistance. Cardiac output was decreased by LNNA. L-Arg, again, did not influence the hemodynamic variables as compared with the vehicle control group. The regional vascular resistance index was increased by LNNA in many tissues and organs, except the brain and the heart. Regional blood flow, on the other hand, was significantly decreased only in the liver and skin by LNNA. The marked reduction in NO₃^- in urine by LNNA-treatments may indicate that the measured NO₃^- is exclusively of endogenous origin, and that inhibition of NO production causes elevation of blood pressure by constricting peripheral arteries. Sympatholytic responses by the baroreceptor reflex were thereby evident only on the second and the third days, which was indicated by bradycardia and suppression of noradrenaline excretion into urine. These results indicate that the inhibition of NO synthase actually decreases production of endogenous NO, and that the hypertension caused by decreases in NO production is due to elevation of total peripheral vascular resistance. (Hypertens Res 1995; 18: 319-324)

収録刊行物

• Hypertension Research

  Hypertension Research 18 (4), 319-324, 1995

  日本高血圧学会

キーワード

• nitric oxide
• nitric oxide synthase inhibitor
• hypertension
• nitrate ion
• catecholamine
• hemodynamics

詳細情報

• CRID: 1390282679697276544
• NII論文ID: 130003456253
• NII論文ID: 30034931648
• NII書誌ID: AA10847079
• DOI: 10.1291/hypres.18.319
• COI: 1:CAS:528:DyaK28XhtFGrt7o%3D
• ISSN: 13484214
• ISSN: 09169636
• ISSN: http://id.crossref.org/issn/09169636
• PubMed: 8747311
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可