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为研究一氧化氮合酶抑制剂左旋硝基精氨酸诱导的肺动脉高压大鼠各部位离体血管环对多巴胺－ １ 受体反应性的影响，采用大鼠肺动脉、肠系膜动脉和肾动脉离体血管标本，在去甲肾上腺素收缩血管后，用多巴胺－ １ 受体选择性激动剂非诺多泮使血管舒张，所有实验在吲哚美辛（１０ μｍｏｌＬ） 和普萘洛尔（３ μｍｏｌＬ） 存在下进行。左旋硝基精氨酸组大鼠各动脉对非诺多泮的反应性均有不同程度的降低，以肺动脉最明显，最大舒张占预收缩的百分比为４５．５％ ±４．１％ ，低于对照组的９７．３ ％ ±１０ ．６ ％（ Ｐ＜ ０．０１）；亲合常数为２０４２ ±２２１，低于对照组的４２７４ ．２±５１２（Ｐ＜ ０．０１） ，接近对照组的去内皮水平。肠系膜动脉和肾动脉对非诺多泮的反应性亦有下降，但下降程度明显低于肺动脉。结果提示，内皮依赖性受体介导多巴胺－ １ 的舒张效应降低是左旋硝基精氨酸形成肺动脉高压的因素之一。
In order to investigate the effect of isolated vascular rings at various parts of rat pulmonary hypertension induced by nitric oxide synthase inhibitor L - NNA on the dopamine - 1 receptor reactivity, rat pulmonary artery, mesenteric artery and renal artery were isolated Vascular samples were vasodilated with fenoldopam, a selective agonist of dopamine - 1 receptor, after norepinephrine constriction of blood vessels. All the experiments were performed on indometacin (10 μmolL) and propranolol (3) μmolL). L-nitroarginine group of rats in each artery of fenofiban reactivity were reduced to varying degrees, the most obvious pulmonary artery, the maximum diastolic pre-contraction percentage was 45.5% ± 4.1%, low 97.3% ± 10 in the control group. 6% (P <0.01). The affinity constant was 2042 ± 221, which was lower than 4274 in the control group. 2 ± 512 (P <0.01), close to the endothelium level of the control group. Mesenteric artery and renal artery reactivity with fenoldopam also decreased, but the decline was significantly lower than the pulmonary artery. The results suggest that reduced endothelium-dependent receptor-mediated dilation of dopamine-1 is one of the factors that cause L-NNA to form pulmonary hypertension.