Mechanisms of noradrenaline‐induced vasorelaxation in isolated femoral arteries of the neonatal rat

Isolated arteries from the femoral circulation of Wistar rats mounted on a small vessel myograph demonstrated age related tension development to noradrenaline (NA, 1×10 −8 –5×10 −5   M ) day 20 greater than day 10 ( P < 0.005); day 100 greater than day 20 ( P < 0.001) and depolarizing potassium (125 m M ) buffer day 20 greater than day 10 ( P < 0.001). NA evoked dilatation in femoral arteries from neonatal rats (10 days) when added to unstimulated vessels or to those preconstricted with the thromboxane mimetic, U46619. Relaxation to NA was inhibited by L ‐NAME (0.1 m M ) ( P < 0.001), endothelial removal ( P < 0.001) and the α 2 ‐adrenoceptor antagonist, yohimbine (0.1 μ M ) ( P < 0.001). α 1 ‐ or β‐adrenoceptor antagonism was without effect. Relaxation was evoked in femoral arteries of the 10‐day‐old rats by the α 2 ‐adrenoceptor agonist UK14304 (1×10 −8 –5×10 −5   M ). This relaxation was also abolished by L ‐NAME (0.1 m M ) ( P < 0.001) or endothelial removal ( P < 0.001). α 2 ‐adrenoceptor‐mediated vasorelaxation was the predominant response to NA stimulation in femoral arteries of the neonatal rat. These responses were endothelium‐dependent and were NO‐mediated. British Journal of Pharmacology (1999) 127 , 809–812; doi: 10.1038/sj.bjp.0702641