抄録
The effects of dilevalol on vascular adrenoceptors were investigated using helical strips of cat arteries. In coronary arteries partially pre-contracted with prostaglandin F2α (PGF2α), the concentration-relaxant response curves for isoproterenol were shifted to the right by dilevalol with a potency similar to that of propranolol, although dilevalol itself did not relax the arteries. Contractions induced by norepinephrine of mesenteric arteries were attenuated by low concentrations of prazosin but were not influenced by yohimbine of up to 10-8M. In contrast, the norepinephrine-induced contractions of middle cerebral arteries were attenuated by yohimbine but only slightly attenuated by prazosin. With mesenteric arteries, treatment with dilevalol (10-7 to 10-5M) attenuated the contractions induced by norepinephrine and phenylephrine in a concentration-dependent manner. On the other hand, contractions induced by norepinephrine and clonidine in middle cerebral arteries were not attenuated by treatment with dilevalol of up to 10-6M. Treatment with low concentrations of dilevalol (10-8 to 10-7M) potentiated the contractile response to the electrical stimulation of adrenergic nerves in mesenteric arteries while high concentrations (3×107 to 105M) attenuated it. The potentiation was reversed to attenuation by pretreatment with propranolol. Treatment with isoproterenol (10-10 to 10-9M) also potentiated the contractile response to the electrical stimulation in the arteries. Isoproterenol did not cause any relaxation of mesenteric arteries precontracted with PGF2α. Attenuations by clonidine of the response to the electrical stimulation in the arteries did not significantly differ in control arteries and those treated with a high concentration (10-6M) of dilevalol. These results suggest that dilevalol has a potent β-receptor blocking activity, weak α1-blocking activity and β-agonistic activity but has no effect on the α2-adrenoceptor. The potentiating effect of dilevalol on the contractile response to adrenergic nerve stimulation seems to occur only in arteries which do not relax with β-agonist.
