| First Author | Vandeputte C | Year | 2002 |
| Journal | Br J Pharmacol | Volume | 135 |
| Issue | 5 | Pages | 1209-12 |
| PubMed ID | 11877328 | Mgi Jnum | J:103201 |
| Mgi Id | MGI:3608727 | Doi | 10.1038/sj.bjp.0704567 |
| Citation | Vandeputte C, et al. (2002) Modulation of contraction by alpha(2A/D)-adrenoceptors in mouse aorta: evidence employing knockout technology. Br J Pharmacol 135(5):1209-12 |
| abstractText | 1. We have investigated noradrenaline-evoked contractions in endothelium-denuded aorta from wild-type and alpha(2A/D)-adrenoceptor knockout mice. The maximum contraction to noradrenaline was significantly larger (1.36 +/- 0.24 mN, n=5) in aorta from knockout than from wild-type animals (0.78 +/- 0.14 mN, n=12, P<0.05), but there was no difference in potency of noradrenaline. There was no difference between groups in the contraction to KCl (80 mM) or PGF(2 alpha) (10 microM). 2. The contraction to noradrenaline (10 microM) was significantly larger in aorta from knockout animals, but yohimbine (1 microM) significantly increased this contraction (to 136 +/- 10% of control, n=6) in aorta from wild-type but not from knockout (97 +/- 10%, n=6, P<0.05). 3. In tissues precontracted with PGF(2 alpha) (10 microM), xylazine (1 microM) produced relaxations only in tissues from wild-type mice. 4. The K(+) channel blocker glibenclamide (1 microM) had no significant effects on contractions to noradrenaline in either group. 5. It is concluded that an alpha(2A/D)-adrenoceptor exerts an inhibitory modulation of contraction in mouse aorta. |
