Experiments were performed to determine the subtypes of alpha-adrenoceptors involved in the contraction induced by rilmenidine in isolated canine cutaneous veins. Rings of saphenous vein (without endothelium) were suspended for the recording of isometric force in physiological salt solution. All experiments were performed in the presence of propranolol (to antagonize beta-adrenoceptors), cocaine (to inhibit neuronal uptake) and hydrocortisone (to inhibit extraneuronal uptake). In the presence of rauwolscina (an alpha2-adrenegic blocker), rilmenidine caused concentration-dependent contractions which were inhibited by prazosin (nonselective alpha1-antagonist) and by (+)niguldipine (selective alpha(1A)-adrenergic antagonist), but not by (-)nigurdipine. After treatment with phenoxybenzamine (to alkylate alpha1-adrenoceptors), rilmenidine evoked contractions of the canine saphenous vein which were antagonized competitively by rauwolscine. The combination of rauwolscine and prazosin did not abolish contractions evoked by the highest concentrations of rilmenidine. Although binding experiments using 3H-idazoxan suggested the existence of a nonadrenergic binding site (around 20% of the total binding), contractile studies failed to demonstrate their involvement in the increases in tension evoked by rilmenidine. These experiments suggest that the contractions evoked by rilmenidine in isolated canine veins are mediated by both alpha(1A)- and alpha2-adrenoceptors.
Rilmenidine activates postjunctianal alpha1- and alpha2-adrenoceptors in the canine saphenous vein
TADDEI, STEFANO;
1996-01-01
Abstract
Experiments were performed to determine the subtypes of alpha-adrenoceptors involved in the contraction induced by rilmenidine in isolated canine cutaneous veins. Rings of saphenous vein (without endothelium) were suspended for the recording of isometric force in physiological salt solution. All experiments were performed in the presence of propranolol (to antagonize beta-adrenoceptors), cocaine (to inhibit neuronal uptake) and hydrocortisone (to inhibit extraneuronal uptake). In the presence of rauwolscina (an alpha2-adrenegic blocker), rilmenidine caused concentration-dependent contractions which were inhibited by prazosin (nonselective alpha1-antagonist) and by (+)niguldipine (selective alpha(1A)-adrenergic antagonist), but not by (-)nigurdipine. After treatment with phenoxybenzamine (to alkylate alpha1-adrenoceptors), rilmenidine evoked contractions of the canine saphenous vein which were antagonized competitively by rauwolscine. The combination of rauwolscine and prazosin did not abolish contractions evoked by the highest concentrations of rilmenidine. Although binding experiments using 3H-idazoxan suggested the existence of a nonadrenergic binding site (around 20% of the total binding), contractile studies failed to demonstrate their involvement in the increases in tension evoked by rilmenidine. These experiments suggest that the contractions evoked by rilmenidine in isolated canine veins are mediated by both alpha(1A)- and alpha2-adrenoceptors.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
