Abstract
Pharmacological properties of the facilitatory presynaptic β-adrenoceptor mechanism were studied in superfused spiral preparations of guinea-pig pulmonary arteries preloaded with 3H-norepinephrine. (-)-lsoproterenol (0.3 μM)-induced increases in total 3H efflux per pulse evoked by transmural field stimulation (1, 5, 10 and 20 Hz, 10 V, 2 msec pulse width, 100 pulses and 30 min intervals) were neither dependent on impulse-frequencies nor selective at lower frequencies. Isoproterenol increased 3H efflux at 5 Hz in a concentration-dependent manner (1 nM to 1 μM): pD2 was 7.7. Salbutamol increased 3H efflux in a similar manner to isoproterenol: pD2 was 7.4. Prenalterol at 3 μM only slightly increased 3H efflux. Tazolol (10 nM to 3 μM) produced no increases. Atenolol (3 μM) and practolol (3 μM) did not antagonize isoproterenol (0.3 μM)-induced increases in 3H efflux. Butoxamine (3 μM) and H 35/25 (3 μM) did antagonize this parameter. (-)-Epinephrine (1 nM to 0.1 μM) decreased 3H efflux at 5 Hz and concentration-dependently increased this parameter in the presence of 10 μM phentolamine. (-)-Norepinephrine (10 nM to 1 μM) concentration-dependently inhibited evoked 3H efflux and did not increase the parameter in the presence of 10 μM phentolamine, 10 μM cocaine and 10 μM normetanephrine. Thus, there exist presynaptic β2-subtype receptors on noradrenergic nerve endings innervating guinea-pig pulmonary arteries.
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