Nitric oxide contributes to AT2 but not AT1 angiotensin II receptor-mediated vasodilatation of porcine pial arteries and arterioles

作者: Dimitry Baranov , William M. Armstead

DOI: 10.1016/J.EJPHAR.2005.06.052

关键词:

摘要: Abstract Angiotensin II elicits pial artery dilation by activating angiotensin AT 1 and 2 receptors. This study determined if vasodilatation in response to receptor activation is due stimulated release of nitric oxide (NO) newborn pigs equipped with a closed cranial window. (10 − 8 , 10 6 M) elicited dilatation that was unchanged the NO synthase inhibitor N ϖ-Nitro- l -Arginine ( -NNA) (12 ± 3 18 ± 2 versus 12 ± 3 21 ± 4%). not associated changes artificial cerebrospinal fluid (CSF) cGMP concentration, an indicator release. Similar data were obtained for agonist L 162,313. In contrast, CGP 42112A induced blocked -NNA (9 ± 2 18 ± 3 1 ± 1 1 ± 1%). elevated CSF concentration (757 ± 18, 1590 ± 89, 2101 ± 116 fmol/ml) such -NNA. These indicate contributes but vasodilatation. suggest primarily via activation.

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