Presynaptic P1‐purinoceptors in jejunal branches of the rabbit mesenteric artery and their possible function.
Presynaptic P1‐purinoceptors in jejunal branches of the rabbit mesenteric artery and their possible function.
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DOI：
10.1113/jphysiol.1988.sp016985
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发表时间：
1988-03
期刊：
影响因子：
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通讯作者：
P. Illés;R. Jackisch;J. Regenold
中科院分区：
文献类型：
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作者：
P. Illés;R. Jackisch;J. Regenold
1.在兔肠系膜动脉平滑肌细胞上记录到15次1 Hz脉冲刺激诱发的兴奋性连接电位(EBP)。测定了P1-嘌呤受体激动剂和拮抗剂以及干扰内源性腺苷失活的物质的作用。2.腺苷及其类似物以浓度依赖的方式抑制列车内的EchP。第一个EJP的抑制率与后一个的相似，但一些早期的EJP被抑制得更明显。激动剂的效价顺序为(-)-N6-(R-苯基异丙基)-腺苷(R-PIA)>(+)-N6-(S苯异丙基)-腺苷(S-PIA)>腺苷。3.8-苯基茶碱(1，10mumol/L)、8-环戊基茶碱(0.1mumol/L)和8-(对磺苯基)-茶碱(100mumol/L)3种甲基黄嘌呤可拮抗R-PIA的作用。当单独给予时，它们也增强了列车中所有EBP的幅度。第一个EJP和后一个EJP的易化百分比相似。然而，一些早期的EBP得到了更明显的增强。8-苯基茶碱在预防R-PIA的作用和增强EchP方面均弱于8-环戊基茶碱。强烈拮抗R-PIA效应的8-(对磺苯基)-茶碱(100mumol/L)对EjP仅有适度的易化作用。4.S-(对-硝基苄基)-6-硫代鸟苷(10摩尔/L)均能抑制ECPs，并增强腺苷的抑制作用。腺苷脱氨酶(10微克/毫升)可引起一定程度的EBP增强；这种作用可被浓度为10摩尔/L的脱氧考福霉素所阻断，而该作用本身并无作用。AH21-132(10Mumol/L)增强了列车内所有的EBP。5.上述物质均不影响血管内皮细胞静息膜电位。此外，R-PIA(0.1mumol/L)不改变去甲肾上腺素(3mumol/L)引起的去极化。6.我们认为兔肠系膜动脉节后交感神经元的轴突终末含有A1型的P_1-嘌呤受体。内源性腺苷激活这些突触前受体可能会抑制主要神经效应递质的释放，可能是ATP。
1. Excitatory junction potentials (EJPs) evoked by nerve stimulation with fifteen pulses at 1 Hz were recorded from smooth muscle cells of the rabbit isolated mesenteric artery. The effects of P1‐purinoceptor agonists and antagonists, as well as of substances which interfere with the inactivation of endogenous adenosine, were tested. 2. Adenosine and its analogues depressed the EJPs in the train in a concentration‐dependent manner. The percentage inhibition of the first EJP and that of the later ones was similar; some early EJPs, however, were inhibited more markedly. The rank order of potency of the agonists was (‐)‐N6‐(R‐phenylisopropyl)‐adenosine (R‐PIA) congruent to 5'‐N‐ethylcarboxamidoadenosine (NECA) greater than (+)‐N6‐(S‐phenylisopropyl)‐adenosine (S‐PIA) greater than adenosine. The respective IC40 values (the concentrations producing 40% inhibition of the first EJP in the train) were 0.018, 0.028, 0.83 and 4.7 mumol/l. 3. Three methylxanthines, namely 8‐phenyltheophylline (1, 10 mumol/l), 8‐cyclopentyltheophylline (0.1, 1 mumol/l) and 8‐(p‐sulphophenyl)‐theophylline (100 mumol/l), antagonized the effect of R‐PIA (0.1 mumol/l). When given alone they also enhanced the amplitudes of all EJPs in the train. The percentage facilitation of the first EJP and that of the later ones was similar. Some early EJPs, however, were potentiated more markedly. 8‐Phenyltheophylline was less potent than 8‐cyclopentyltheophylline both in preventing the action of R‐PIA and in enhancing the EJPs. A concentration (100 mumol/l) of 8‐(p‐sulphophenyl)‐theophylline, which strongly antagonized the R‐PIA effect, produced only a moderate facilitation of EJPs. 4. S‐(p‐nitrobenzyl)‐6‐thioguanosine (10 mumol/l) both depressed the EJPs, and enhanced the inhibitory effect of adenosine. Adenosine deaminase (10 micrograms/ml) caused some potentiation of EJPs; this action was prevented by a concentration (10 mumol/l) of deoxycoformycin, which had no effect of its own. AH21‐132 (10 mumol/l) enhanced all EJPs in the train. 5. None of the above substances influenced the resting membrane potential of the smooth muscle cells. In addition, R‐PIA (0.1 mumol/l) did not change the depolarization induced by noradrenaline (3 mumol/l). 6. We suggest that the axon terminals of postganglionic sympathetic neurones in the rabbit mesenteric artery possess P1‐purinoceptors of the A1‐type. The activation of these presynaptic receptors by endogenous adenosine may inhibit the release of the main neuroeffector transmitter, which is probably ATP.(ABSTRACT TRUNCATED AT 400 WORDS)