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Responsiveness to noradrenaline in aorta from wild-type, nitric oxide synthase-2, nitric oxide synthase-3 and α 2A/D -adrenoceptor knockout mice

European Journal of Pharmacology, ISSN: 0014-2999, Vol: 466, Issue: 1, Page: 129-136
2003
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We have investigated the responsiveness of mouse aorta to noradrenaline (10 μM). In wild-type mice, noradrenaline produced an initial peak contraction (3.35±0.28 mN) and a significantly smaller plateau response (2.15±0.41 mN). The contractions were similar in aorta from nitric oxide synthase-2 (NOS-2) knockout mice. In vessels from NOS-3 knockout mice, noradrenaline contractions consisted of an early steeply rising phase with a later shallow rising phase to a maximum (10.21±0.84 mN), which was significantly greater than in wild-type and NOS-2 knockout mice, and resembled the contraction to phenylephrine (10 μM) in wild-type. In α 2A/D -adrenoceptor knockout mice, the noradrenaline maximum was significantly smaller than in NOS-3 knockout but significantly larger than in wild-type. Following N G -nitro- l -arginine methyl ester ( l -NAME, 10 μM), responses in wild-type and α 2A/D -adrenoceptor knockout were as in NOS-3 knockout mice. The α 2D -adrenoceptor antagonist BRL 44408 (2-((4,5-dihydro-1 H -imidazole-2-yl)methyl)-2,3-di-hydro-1-methyl-1 H -isoindole maleate; 1 μM) increased noradrenaline-induced contractions and the α 2 -adrenoceptor agonist xylazine reduced Prostaglandin F 2α -induced contractions, in wild-type but not NOS-3 knockout. Contractions to noradrenaline in mouse aorta are modulated by NOS-3 and part of the effect involves activation of α 2A/D -adrenoceptors.

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