THE INHIBITORY EFFECT OF OPIOID-PEPTIDES AND MORPHINE APPLIED INTRATHECALLY AND INTRACEREBROVENTRICULARLY ON THE MICTURITION REFLEX IN THE CAT
THE INHIBITORY EFFECT OF OPIOID-PEPTIDES AND MORPHINE APPLIED INTRATHECALLY AND INTRACEREBROVENTRICULARLY ON THE MICTURITION REFLEX IN THE CAT
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DOI：
10.1016/0006-8993(84)91146-6
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发表时间：
1984-01-01
期刊：
影响因子：
2.9
通讯作者：
DEGROAT, WC
中科院分区：
文献类型：
--
作者：
HISAMITSU, T;DEGROAT, WC
鞘内（i.t.）和脑室内（i. c. v.）脑啡肽和脑啡肽类似物的给药抑制[猫]膀胱的反射收缩和膀胱副交感节后神经的放电。亮氨酸-和甲硫氨酸-脑啡肽（L-Enk和M-Enk，平均阈值剂量：110 μ g，i.t.和17 μ g，i.c.v.）引起短暂的持续抑制（3-30分钟），而D-Ala-亮氨酸-和D-Ala 2-甲硫氨酸脑啡酰胺（平均阈值剂量23 μ g，i.t.），抑制作用更强，持续时间更长（1.5- 3 n）。DSLET [酪氨酰-D-丝氨酰-甘氨酰苯丙氨酰-亮氨酰苏氨酸]，a.选择性阿片受体激动剂，当i. c. v.或i.t. (mean阈值剂量0.08和13 μ g），而吗啡对μ g具有更大的亲和力。通过i. c. v.和静脉内（i. v.）注射（平均阈值剂量，5和300 μ g/kg），但不通过i.t.注射液（200-400 μ g）。Thiorphan（50-200 μ g i.t.，i.c.v.）增强了对L-Enk的应答，而纳洛酮（10-50 μ g，i.t.，静脉注射，i.v.），阻断了对所有阿片类物质的反应。在未治疗的动物中，thiorphan抑制膀胱反射，纳洛酮增强膀胱反射。在i.t.给药纳洛酮（10-200 μ g）增加了膀胱收缩的持续时间和幅度，而i. c. v.注射时，药物增加了收缩的频率并降低了收缩的幅度。注射大剂量纳洛酮，但不是静脉注射，产生持续的膀胱收缩和膀胱传出放电。结果表明，膀胱反射是由紧张性脑啡肽能抑制机制在大脑和脊髓。在脑中，脑啡肽能抑制由δ介导。和μ。阿片受体似乎控制膀胱收缩的频率和排尿阈值，而在脊髓中，抑制由δ介导。受体，似乎控制膀胱收缩的幅度。
Intrathecal (i.t.) and intracerebroventricular (i.c.v.) administration of enkephalins and enkephalin analogs inhibited reflex contractions of the [cat] urinary bladder and firing in vesical parasympathetic postganglionic nerves. Leucine- and methionine-enkephalin (L-Enk and M-Enk, mean threshold doses: 110 .mu.g, i.t. and 17 .mu.g, i.c.v.) elicited short-lasting inhibition (3-30 min), whereas D-Ala-leucine- and D-Ala2-methionine enkephalinamide (mean threshold dose 23 .mu.g, i.t.), produced more prominent and prolonged inhibition (1.5-3n). DSLET [tyrosyl-D-seryl-glycylphenylalanyl-leucylthreonine], a .delta. selective opiate receptor agonist, blocked bladder activity when injected i.c.v. or i.t. (mean threshold doses 0.08 and 13 .mu.g), whereas morphine, which has greater affinity for .mu. opiate receptors, was effective by i.c.v. and intravenous (i.v.) injection (mean threshold doses, 5 and 300 .mu.g/kg), but not by i.t. injection (200-400 .mu.g). Thiorphan (50-200 .mu.g i.t., i.c.v.) enhanced the responses to L-Enk, whereas naloxone (10-50 .mu.g, i.t., i.c.v., i.v.), blocked the responses to all opioid substances. In untreated animals thiorphan depressed and naloxone enhanced bladder reflexes. Within i.t. administration naloxone (10-200 .mu.g) increased the duration and magnitude of bladder contractions, whereas with i.c.v. injections, the drug increased the frequency and reduced the amplitude of the contractions. Large doses of naloxone i.t., but not i.c.v., produced sustained bladder contractions and vesical efferent firing. The results indicate that bladder reflexes are controlled by tonic enkephalinergic inhibitory mechanisms in both the brain and spinal cord. In the brain enkephalinergic inhibition which was mediated by .delta. and .mu. opiate receptors, seems to control the frequency of bladder contractions and micturition threshold, whereas in the spinal cord, inhibition is mediated by .delta. receptors and seems to control the magnitude of bladder contractions.