influence of endo thelium removal and lname on responses of rat common carotid artery to α-adrenoceptor agonists

in this study we investigated the effects of endothelium removal and l-name on responses to α-adrenoceptor agonists. male wistar rats were killed by overdose with pentobarbitone sodium, after which the left and right common carotid arteries were removed. rings of arteries 3-4 mm in length were cut from each vessel and then mounted in 10 ml isolated organ bath, bathed in krebs maintained at 37°c and gassed with 95% 02 plus 5% co2, the preparations were allowed to equilibrate for an hour. l-name was added approximately 10-15 min prior to the onset of cumulative concentration-response curves (ccrc) to an agonist. in some preparations the endothelial layer was removed mechanically by gently rolling the tissue around a thin wire. removal of the endothelium was confirmed pharmacologically by a lack of relaxant response to the potent endotheliumdependent vasodilator acetylcholine. inhibition of no synthesis by l-name results in significant vasoconstriction. l-name prevented the relaxation of rat carotid artery by acetylcholine, suggesting that both basal and stimulated release of nitric oxide can regulate vascular tone in this artery. mechanical disruption of the vascular endothelium reduced, but did not abolish, the ability of l-name to produce contraction. this suggests an extra-endothelial site for nitric oxide synthesis in rat common carotid artery. inhibition of nitric oxide synthase with lname potentiated responses to phenylephrine and uk-14304 but not to noradrenaline. mechanical disruption of the vascular endothelium potentiated responses to uk-14304, phenylephrine and noradrenaline. we suggest that constitutive no activity has substantial inhibitory influence on vasoconstrictor responses to phenylephrine and uk-14304 but not to noradrenaline.