The membrane potential of vascular smooth muscle appears to modulate uptake2 of 3H-isoprenaline.

Segments of the rabbit main pulmonary artery and of its two branches were exposed for 10 min to 50 nmol/l 3H-(+/-)-isoprenaline, and the accumulation of tritium in the tissue was determined; COMT was inhibited in all experiments. 1. The accumulation of the tritium label was sensitive to 3-O-methyl-isoprenaline (OMI), showing that this vascular smooth muscle possesses uptake2. 2. In the presence of 0.01 to 1 mumol/l (-)-noradrenaline, the accumulation of tritium was depressed (in a concentration-dependent manner). This decline involved the OMI-sensitive accumulation of 3H-isoprenaline. 3. The presence of any one of three selective alpha 1-adrenoceptor antagonists (1 mumol/l prazosin, 1 mumol/l WB4101, 10 mumol/l corynanthine) prevented the effect of 1 mumol/l (-)-noradrenaline on the accumulation of tritium. However, in the absence of (-)-noradrenaline, the three antagonists failed to affect the accumulation of tritium. 4. 10 mumol/l nicorandil caused the accumulation of tritium to increase. 5. As stimulation of alpha 1-adrenoceptors is known to result in depolarization, and as nicorandil is known to hyperpolarize this smooth muscle, it is concluded that the resting membrane potential modulates uptake2.