Fernandes Liliam, Loiola Rodrigo Azevedo, Tostes Rita C A, Nigro Dorothy, Fortes Zuleica Bruno, de Carvalho Maria Helena Catelli
Department of Pharmacology, Institute of Biomedical Sciences I-s/213, University of São Paulo, Av. Prof. Lineu Prestes 1524, 05508 900 São Paulo, SP, Brazil.
Peptides. 2005 Dec;26(12):2458-63. doi: 10.1016/j.peptides.2005.05.025. Epub 2005 Jul 25.
The venoconstrictor effect of Angiotensin II (Ang II) was investigated in the rat mesenteric venules and portal vein. Mesenteric venules were perfused at a constant rate and reactivity to Ang II (0.1 nmol) was evaluated as changes in the perfusion pressure. Rings of portal vein were mounted in organ baths and curves to Ang II (0.1-100 nmol/L) were generated. In venules, Ang II-contraction (10.6+/-1.1 mmHg) was abolished by losartan (0.9+/-0.3 mmHg*), reduced by PD 123,319 (5.8+/-0.9 mmHg*), increased by L-NAME (16.5+/-1.8 mmHg*) and not altered by indomethacin. In portal veins, curves to Ang II (-logEC50: 8.9+/-0.1 mol/L) were shifted to the right by losartan (-log EC50: 7.5+/-0.1 mol/L*) and by PD 123,319 (-logEC50: 8.0+/-0.1 mol/L*). L-NAME increased the maximal response to Ang II (Emax: 0.91+/-0.1g versus 1.62+/-0.3g*) and indomethacin had no effect. In conclusion, Ang II induces venoconstriction by activating AT1 and AT2 receptors. Data obtained with L-NAME provide evidence that the basal nitric oxide release from the endothelium of the venous system can modulate the Ang II-induced venoconstriction.
在大鼠肠系膜小静脉和门静脉中研究了血管紧张素II（Ang II）的静脉收缩作用。以恒定速率灌注肠系膜小静脉，并将对Ang II（0.1 nmol）的反应性评估为灌注压力的变化。将门静脉环安装在器官浴槽中，并生成对Ang II（0.1 - 100 nmol/L）的量效曲线。在小静脉中，氯沙坦可消除Ang II诱导的收缩（10.6±1.1 mmHg）（降至0.9±0.3 mmHg*），PD 123,319可使其降低（降至5.8±0.9 mmHg*），L - NAME可使其增强（升至16.5±1.8 mmHg*），而吲哚美辛则无影响。在门静脉中，氯沙坦（-log EC50：7.5±0.1 mol/L*）和PD 123,319（-logEC50：8.0±0.1 mol/L*）可使Ang II的量效曲线（-logEC50：8.9±0.1 mol/L）右移。L - NAME增加了对Ang II的最大反应（Emax：0.91±0.1g对1.62±0.3g*），吲哚美辛则无作用。总之，Ang II通过激活AT1和AT2受体诱导静脉收缩。L - NAME获得的数据表明，静脉系统内皮细胞基础一氧化氮释放可调节Ang II诱导的静脉收缩。
