Investigations into the mechanism of morphine and ethanol inhibition in the guinea pig ileum longitudinal muscle strip

1980 ◽  
Vol 58 (3) ◽  
pp. 265-270 ◽  
Author(s):  
John G. Clement

It has been noted that the analgesic property of ethanol bears a marked resemblance to that of morphine. The purpose of this study was to determine if the mechanism of action of morphine and ethanol was similar using the guinea pig ileal longitudinal muscle strip (GPI-LMS). Ethanol (35–260 mM) depressed the twitch response and the acetylcholine- (ACh-), KCl-, and BaCl2-induced contractions to the same extent while having no significant effect on the binding of [3H]quinuclidinyl benzilate ([3H]QNB) to muscarinic receptors. Morphine (53–530 nM) inhibited the twitch response and to a lesser extent BaCl2- and KCl-induced contractions while having no significant effect on either ACh-induced contractions or the binding of [3H]QNB to muscarinic receptors. Naloxone and increased [Ca2+] reversed the inhibitory effects of morphine but not ethanol. Ethanol appears to inhibit a site after interaction of ACh with the receptor. Mechanism of inhibition of BaCl2 response is also different as naloxone and increased [Ca2+] reverse morphine but not ethanol inhibition. Ethanol inhibition in GPI-LMS does not involve the opiate receptor.

1982 ◽  
Vol 60 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Y. H. Kwok ◽  
F. Mitchelson

The antimuscarinic activity of amitriptyline, mianserin, and viloxazine was compared with atropine in guinea-pig ileal longitudinal muscle. The pA2 values obtained using carbachol (CCh) as agonist were as follows: atropine, 9.55; amitriptyline, 7.50; mianserin, 6.40; and viloxazine, 4.91. Responses to transmural electrical stimulation (1–50 Hz) were more resistant than those produced by CCh to inhibition by atropine and the antidepressants. This did not appear to be due to a selective inhibition of prejunctional inhibitory muscarinic receptors, as a pA2 of 8.73 was obtained with atropine for the depression of oxotremorine-induced inhibition of acetylcholine (ACh) output. Amitriptyline (10 μM) caused a 2.4-fold increase in ACh output and was 200-fold weaker than atropine at doubling ACh output in the longitudinal muscle stimulated at 0.3 Hz. Mianserin (10 μM) and viloxazine (1–10 μM) did not significantly affect ACh output. It is suggested that the antidepressants exhibit a greater affinity for the postjunctional muscarinic receptors in the guinea-pig ileal longitudinal muscle.


1983 ◽  
Vol 89 (3-4) ◽  
pp. 229-234 ◽  
Author(s):  
Eiichi Hayashi ◽  
Kazumasa Shinozuka ◽  
Toshio Maeda ◽  
Mitsuhiro Takeda

1982 ◽  
Vol 79 (3-4) ◽  
pp. 245-255 ◽  
Author(s):  
Ondřej Kadlec ◽  
Isidor Šeferna ◽  
Karel Mašek ◽  
George T. Somogyi ◽  
Joseph Knoll

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