Maas A J, Den Hertog A
Eur J Pharmacol. 1980 Mar 21;62(2-3):157-66. doi: 10.1016/0014-2999(80)90272-1.
In the taenia of guinea-pig caecum, electrical stimulation of the non-adrenergic inhibitory nerves caused relaxation which was followed by an after-contraction. The purinergic compount ATP (10(-5) M) also produced muscle relaxation while wash-out was associated with an after-contraction. The role of prostaglandins (E1, E2, F1 alpha, F2 alpha; 10(-9)--10(-6 M) in these contractions was studied. The prostaglandin responses reflected by membrane depolarization (E type) and muscle contraction (E and F type) were inhibited by the phenyl phosphonate N-0164 (10(-5) M). This substance did not affect the membrane potential or the nerve-mediated non-adrenergic inhibitory junction potential (IJP). The effect of N-0164 on the muscle cells could account for the limited reduction of the after-depolarization and contraction following electrical stimulation. The ATP after-contraction, however, could be inhibited completely by N-0164. The results are consistent with the possibility that the ATP after-contraction was produced by E type prostaglandins, while involvement of prostaglandins in post inhibitory excitation following nerve stimulation seems unlikely.
在豚鼠盲肠的带状肌中,电刺激非肾上腺素能抑制神经会引起松弛,随后出现后收缩。嘌呤能化合物ATP(10⁻⁵M)也会使肌肉松弛,而冲洗后则会出现后收缩。研究了前列腺素(E1、E2、F1α、F2α;10⁻⁹ - 10⁻⁶M)在这些收缩中的作用。由膜去极化反映的前列腺素反应(E型)和肌肉收缩(E型和F型)受到苯基膦酸酯N - 0164(10⁻⁵M)的抑制。该物质不影响膜电位或神经介导的非肾上腺素能抑制性接头电位(IJP)。N - 0164对肌肉细胞的作用可以解释电刺激后去极化和收缩的有限减少。然而,N - 0164可以完全抑制ATP后收缩。结果表明,ATP后收缩可能是由E型前列腺素产生的,而前列腺素似乎不太可能参与神经刺激后的抑制后兴奋。