Effects of prostaglandin I 2 and carbocyclic thromboxane A 2 on smooth muscle cells and neuromuscular transmission in the guinea‐pig mesenteric artery

1 In the guinea‐pig mesenteric arteries neither prostacyclin (PGI 2 ) nor carbocyclic thromboxane A 2 (cTxA 2 ) affected membrane potential in concentrations below 1 × 10 −6 m . Increasing the concentration to 3 × 10 −6 m either slightly hyperpolarized or depolarized the membrane with little change in membrane resistance. 2 At a concentration of 1 × 10 −7 m , the amplitude of the first e.j.p. and the enlarged amplitudes of the subsequent e.j.ps evoked by trains of stimuli were reduced consistently by PGI 2 or cTxA 2 . Facilitation was unaffected by either agent. 3 The inhibitory actions of PGI 2 were partly overcome by increased concentrations of 5 m m [Ca] o and were accelerated by a reduced concentration of 1.25 m m [Ca] o . 4 The amplitude of the contraction evoked by perivascular nerve stimulation was inhibited to a greater extent by PGI 2 than by cTxA 2 at concentrations below 1 × 10 −6 m . 5 The contraction evoked by 5 × 10 −6 m noradrenaline (NA) or excess concentrations of 20.2 m m [K] o was enhanced by 1 × 10 −8 m — 1 × 10 −6 m cTxA 2 and suppressed by 1 × 10 −8 m — 1 × 10 −6 m PGI 2 . The minimum concentration of cTxA 2 required to produce the contraction was 1 × 10 −8 m . 6 These results indicate that transmission at the neuromuscular junction was inhibited consistently by PGI 2 or cTxA 2 , presumably due to inhibition of NA release by suppression of the Ca influx at the nerve terminals. Whereas PGI 2 inhibited, cTxA 2 enhanced the mechanical response by a direct action on the smooth muscle cells.