Pertussis toxin effects on transmitter release from perivascular nerve terminals.

Pertussis toxin (PT) was used to investigate the possible involvement of an inhibitory GTP-binding protein (G protein) in neuromuscular transmission at the sympathetic nerve terminal of guinea pig mesenteric artery. When the intracellular microelectrode technique was used, the amount of transmitter released was evaluated by recording the amplitude of excitatory junction potentials (EJPs) in the vascular smooth muscle (VSM) cells. EJPs were evoked by perivascular nerve stimulation with brief square pulses. The amplitude of EJPs was depressed by exogenously applied norepinephrine (NE) (greater than or equal to 10(-7) M) or histamine (greater than or equal to 10(-7) M). However, these effects of NE and histamine on EJP amplitude were almost completely blocked in PT-pretreated VSM cells (2 x 10(-7) g/ml PT, 24 h at 21 degrees C). These effects of PT pretreatment were time and temperature dependent. In contrast, there was no significant change in the resting membrane potential (-70.1 +/- 2.1 mV) or input resistance (11.9 +/- 0.4 M omega) in the VSM cells after PT pretreatment. These results suggest that the effects of NE and histamine on EJP amplitude may be mediated by PT-sensitive G proteins in the presynaptic nerve terminal.