Effect of isoprenaline on noradrenaline release from sympathetic neurones in rabbit isolated pulmonary artery.

The aim of the present work was to demonstrate the presence of presynaptic beta-adrenoceptors in the rabbit isolated pulmonary artery by investigating the effect of isoprenaline on 3H-noradrenaline (3H-NA) release evoked by electrical field stimulation. (-)-Isoprenaline (10(-7)-10(-6) mol/l) had no effect on the 3H-overflow evoked by stimulation (3 Hz) of the pulmonary artery preloaded with 3H-NA. At 10(-5) mol/l, (-)-isoprenaline reduced the 3H-overflow by maximally 39%. (-)-Isoprenaline (10(-5) mol/l) caused an inhibition that remained almost constant with time. The same results were obtained with (-)-isoprenaline (10(-7)-3 X 10(-5) mol/l) in the presence of cocaine (3 X 10(-5) mol/l), corticosterone (4 X 10(-5) mol/l), and the catechol-O-methyltransferase inhibitor U-0521 (3',4'-dihydroxy-2-methylpropiophenone) (10(-4) mol/l). In the presence of cocaine plus corticosterone, (-)-isoprenaline (3 X 10(-10)-10(-7) mol/l) had no effect on the 3H-overflow evoked by stimulation at 1 Hz. At 10(-6) mol/l, (-)-isoprenaline slightly reduced the 3H-overflow. At 10 Hz, (-)-isoprenaline (10(-6)-3 X 10(-5) mol/l) decreased the 3H-overflow and had no effect at 10(-7) mol/l. In the presence of either rauwolscine (10(-6) mol/l), phentolamine (10(-6) mol/l) or the phosphodiesterase inhibitor ICI 63,197 (3 X 10(-5) mol/l), (-)-isoprenaline (10(-7)-10(-6) mol/l) did not enhance the stimulation-evoked 3H-overflow. (+/-)-Propranolol (10(-7)-10(-5) mol/l) did not alter the stimulation-evoked 3H-overflow.(ABSTRACT TRUNCATED AT 250 WORDS)