• Catherine Vandeputte, P Aiden McCormick, and James R Docherty.
• Department of Physiology, Royal College of Surgeons in Ireland, 2, Dublin, Ireland.
• Eur. J. Pharmacol. 2003 Apr 11;466(1-2):129-36.

AbstractWe have investigated the responsiveness of mouse aorta to noradrenaline (10 microM). 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 microM) in wild-type. In alpha(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 microM), responses in wild-type and alpha(2A/D)-adrenoceptor knockout were as in NOS-3 knockout mice. The alpha(2D)-adrenoceptor antagonist BRL 44408 (2-((4,5-dihydro-1H-imidazole-2-yl)methyl)-2,3-di-hydro-1-methyl-1H-isoindole maleate; 1 microM) increased noradrenaline-induced contractions and the alpha(2)-adrenoceptor agonist xylazine reduced Prostaglandin F(2alpha)-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 alpha(2A/D)-adrenoceptors.

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