Adrenal involvement in captopril-induced potentiation of morphine analgesia
TL;DR: Althoughcaptopril could inhibit the plasma angiotensin-converting enzyme activity, it appeared to have no significant effect on the brain enzyme, and it has been suggested that the effects of captopril and angiotENSin II on morphine analgesia are mediated indirectly through their effects on adrenal function.
About: This article is published in European Journal of Pharmacology.The article was published on 1982-11-19. It has received 11 citations till now. The article focuses on the topics: Captopril & Angiotensin II.
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TL;DR: Captopril has antinociceptive properties, increasing analgesic effect of morphine, and preventing tolerance development, which may occur by suppressing inflammation and ER-stress pathways.
14 citations
TL;DR: Research evidence supports the notion that Ang II acts as anti-opioid peptide to decrease the actions of opioids, and co-administration of ACE inhibitors with opioids exhibits significant interactions possibly due to decreased metabolism of opioids leading to potentiation of their actions.
14 citations
Journal Article•
TL;DR: In morphine group, the number of active lever pressing was significant higher than passive during all 5 days and was also significantly higher than saline group, and the interaction between captopril and opioid system in NAC is highlighted.
Abstract: With an aim to investigate the effects of injection of angiotensin II (Ang II) and captopril into the nucleus accumbens (NAC) on morphine self-administration, male Wistar rats were first trained to receive small pellets of food by pressing the active lever in self-administration apparatus. The animals, divided into 4 groups (saline, morphine, captopril and Ang II) were placed in self-administration apparatus and were allowed to self-administer morphine (0.5 mg per infusion all test groups) or saline (saline group) during consecutive days, for 2 h/sessions. Captopril (30 microg) and Ang II (0.25 nM) were injected into NAC in the corresponding groups before each session. In morphine group, the number of active lever pressing was significantly higher than passive during all 5 days and was also significantly higher than saline group. In captopril group, there were no significant differences between the number of active and passive lever pressings. However, the number of active lever pressing was significantly lower than morphine group. The results highlight the interaction between captopril and opioid system in NAC.
11 citations
TL;DR: Sprague-Dawley rats received oral doses of enalapril maleate, a potent, nonsulfhydryl, angiotensin converting enzyme inhibitor, or saline, and enAlapril did not exhibit analgesic activity nor did it potentiate morphine analgesia.
10 citations
TL;DR: It is concluded, that short-term treatment with captopril or enalapril is not perceived differently by healthy volunteers than placebo or no treatment at all, and the cough associated with ACE-inhibition may be dependent on the duration of treatment, and two weeks was apparently too short for it to emerge.
Abstract: Two randomised, double-blind, cross-over studies inhealthy volunteers given captopril 50 mg b. d. (n = 37; Study I) or enalapril 20 mg o. d. (n = 40; Study 2) and placebo for 2 weeks have been done to examine general well-being. Subjective experiences were evaluated using the standardised, Minor Symptoms Evaluation-profile (MSEP), which was completed during Run-in and on Days l, 4,7 and 14 in the morning.
5 citations
Cites background from "Adrenal involvement in captopril-in..."
...Accumulation of enkephalin within the CNS due to inhibition of the enzyme enkephalinase has been suggested, but this is less likely, since capoten and enalapriI do not readily pass the blood-brain-barrier [15]....
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TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
289,852 citations
TL;DR: The broad substrate specificity of the enzymes suggests that, in addition to the possible contribution of the enzyme to the brain renin‐angiotensin system, other naturally occurring peptides might also be substrates for the enzyme.
Abstract: — Angiotensin converting enzyme of rat brain was studied using Hip-His-Leu as substrate. The highest specific activity of the enzyme was associated with the microsomal fraction. The specific activity of the microsomal enzyme in several regions of the rat brain varied significantly. For example, the specific activities of the striatal and pituitary enzymes were about 10-fold greater than that of the cerebral cortical enzyme. The enzyme required chloride ion; moreover, activity was inhibited in the presence of disodium EDTA or O-phenanthroline, effects suggesting that the converting enzyme of brain is a metalloprotein. SQ-20881, a nonapeptide that inhibits converting enzyme in peripheral tissue, was a potent inhibitor of the enzyme of brain. In addition to Hip-His-Leu, the microsomal fraction was capable of liberating C terminal dipeptides from angiotensin I, Hip-Gly-Gly and Z-Gly- Gly-Val. The broad substrate specificity of the enzyme suggests that, in addition to the possible contribution of the enzyme to the brain renin-angiotensin system, other naturally occurring peptides might also be substrates for the enzyme.
293 citations
TL;DR: Enkephalinase A activity can be completely resolved by DEAE column chromatography from angiotensin converting enzyme activity, demonstrating that they are distinct enzymes.
171 citations
TL;DR: The data indicate that enkephalinase is critically involved in the inactivation of the endogenous opioid peptide released from striatal neurons.
Abstract: Methionine enkephalin release was evoked by depolarization of slices from rat striatum with potassium. In the presence of 0.1 microM thiorphan [(N(R,S)-3-mercapto-2-benzylpropionyl)glycine], a potent inhibitor of enkephalin dipeptidyl carboxypeptidase (enkephalinase), the recovery of the pentapeptide in the incubation medium was increased by about 100 percent. A similar effect was observed with the dipeptide phenylalanylalanine, a selective although less potent enkephalinase inhibitor. Inhibition of other known enkephalin-hydrolyzing enzymes--aminopeptidase by 0.1 mM puromycin or angiotensin-converting enzyme by 1 microM captopril--did not significantly enhance the recovery of released methionine enkephalin. These data indicate that enkephalinase is critically involved in the inactivation of the endogenous opioid peptide released from striatal neurons.
117 citations
TL;DR: The distribution in rat brain of angiotensin converting enzyme using hippuryl-His-Leu as substrate was identical to a dipeptidyl carboxypeptidase present in membranes assayed with Met-enkephalin as substrate.
76 citations