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Abstract-Pharmacologicalproperties of the facilitatory presynaptic i3-adrenoceptor mechanism were studied in superfused spiral preparations of guinea-pig pulmonary arteries preloaded with 3H norepinephrine. (-) Isoproterenol (0.3 /IM) -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 itM): pD2 was 7.7. Salbutamol increased 3H efflux in a similar manner to isoproterenol: pD2 was 7.4. Prenalterol at 3 /LM only slightly increased 3H efflux. Tazolol (10 nM to 3 i M) produced no increases. Atenolol (3 iiM) and practolol (3 i M) did not antagonize isoproterenol (0.3 /N)-induced increases in 3H efflux . Butoxamine (3 ;tM) and H 35/25 (3 /N) did antagonize this parameter.

1 The effects of ( ± )-carteolol 10 8 M to 10-6 M, a non-selective fl-antagonist, applied cumulatively, on stimulation-evoked 3H-release at 1 Hz were studied in pulmonary arteries isolated from guineapigs. The guinea-pigs were subjected to either bilateral adrenalectomy, adrenalectomy followed by injections of deoxycorticosterone acetate (DOCA) and hydrocortisone, bilateral adrenodemedullation or a sham operation, and then loaded in vitro with [3H]-noradrenaline. 2 Carteolol inhibited 3H-output in arteries from sham-operated animals in a concentrationdependent manner. This inhibitory effect was not found in pulmonary arteries from animals subjected to adrenalectomy or adrenodemedullation. However, DOCA and hydrocortisone pretreatment, did not prevent the disappearance of the carteolol-induced inhibition of 3H-release. 3 Adrenalectomy and adrenodemedullation depleted or markedly reduced the endogenous contents of adrenaline in pulmonary arteries without altering the levels of dopamine and noradrenaline. 4 It is concluded that adrenaline, mainly derived from the adrenal medulla, acts as an endogenous agonist for tonically functioning prejunctional fl-adrenoceptors in guinea-pig pulmonary arteries, probably by being taken up and co-released with noradrenaline.

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Abstract-The antagonistic potency, pA2, of several non-selective i3-antagonists on presynaptic (3-adrenoceptors was evaluated using a parallel line assay and MacKay's equation against isoproterenol-induced increases in 3H release in isolated guinea-pig pulmonary arteries preloaded with 3H-norepinephrine. Cumulatively applied isoproterenol at 10-9 M, 10-8 M and 10-7 M dose-dependently increased 3H release evoked by transmural field stimulation at 1 Hz . 19-Antagonists tested dose-dependently antagonized the isoproterenol-induced increases.The order of pA2 was carteolol (11.23+0.09)>nadolol (9.78±0.05)>pindolol (9.59±0.03) >propranolol (9.26±0.17). Carteolol has the highest pA2 and is a useful tool for clarifying whether or not presynaptic (3-adrenoceptors tonically function.