کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2008690 | 1066439 | 2005 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Angiotensin II-induced venoconstriction involves both AT1 and AT2 receptors and is counterbalanced by nitric oxide
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
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 (âlog EC50: 8.9 ± 0.1 mol/L) were shifted to the right by losartan (âlog EC50: 7.5 ± 0.1 mol/L*) and by PD 123,319 (âlog EC50: 8.0 ± 0.1 mol/L*). l-NAME increased the maximal response to Ang II (Emax: 0.91 ± 0.1 g versus 1.62 ± 0.3 g*) 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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Peptides - Volume 26, Issue 12, December 2005, Pages 2458-2463
Journal: Peptides - Volume 26, Issue 12, December 2005, Pages 2458-2463
نویسندگان
Liliam Fernandes, Rodrigo Azevedo Loiola, Rita C.A. Tostes, Dorothy Nigro, Zuleica Bruno Fortes, Maria Helena Catelli de Carvalho,