Kishimoto, T., Aoki, K., Okamiya, Y., Takeshita, T. and Naruchi, T. Effects of clen-buterol on resting tension and contractile response in vesicourethral smooth muscle of rabbits. Jpn. J. Smooth Muscle Res, 25: 13-25, 1989.
The effects of clenbuterol, a selective beta₂-agonist, on isolated smooth muscle prepara-tions from the rabbit bladder body, bladder base and proximal urethra havebeen investigat-ed. The inhibitory effects on resting tension and acetylcholine- and field stimulation-induced contractions in the bladder body werecompared with those of flavoxate, atropine, and verapamil.
Clenbuterol (10^-10-10^-7 M) had a strong, concentration-dependent relaxant effect on resting tension of the bladder body, and the relaxant effect was antagonized bypropranolol. However, clenbuterol had little effect on the bladder base or proximal urethra. Isoproter-enol, a non-selective beta agonist, gave a similar result, but was less potent than clenbuterol. Flavoxate failed to reduce the resting tension, but rather enhanced the spontaneous rhythmic contraction in a concentration-dependent manner. Atropine had little effect. Verapamil produced a concentration-dependent relaxation in the bladder body.
Acetylcholine-induced contraction in the bladder body was completely inhibited by pretreatment with atropine (10^-7 M). Clenbuterol, flavoxate, and verapamil concentration-dependently inhibited acetylcholine-induced contraction. Field stimulation-induced con-traction in the bladder body was not completely inhibited by atropine. However, the residual contraction was completely inhibited by tetrodotoxin. Clenbuterol, flavoxate, and verapamil concentration-dependently inhibited field stimulation-induced contraction. The inhibitory effects of clenbuterol and verapamil were antagonized by an application of propranolol and anincrease in external Ca, respectively.
The data suggest that the selective relaxant effect of clenbuterol on the bladder body is due to beta₂-antagonistic action, resulting in the inhibition of the contractile response to acetylcholine or field stimulation. Also, its response wasdifferent from that of the other drugs used.

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agasaki, M., Yamada, K., Ikezawa, K. and Tamaki, H. Contribution of peripheral opioid receptors to the trimebutine-induced contractions of the proximal colon in anesthetized rats. Japanese Journal of Smooth Muscle Research, 25: 27-30, 1989
In this study we investigated the involvement of opioid receptors in the contractile response to trimebutine using with the proximal colon of anesthetized rats. Trimebutine (3 mg/kg i.v.) enhanced spontaneous contractions of the proximal colon in anesthetized rats. The contractile response was partially inhibited by intravenous administration of an opioid antagonist, naloxone at 1-30μg/kg, but was hardly depressed by intracisternal administra-tion of naloxone (30μg/kg). Morphine (30μg/kg i.v.) evoked colonic contractions which were abolished by intravenous naloxone (30μg/kg). These results suggest that the colonic contractions evoked by trimebutine in anesthetized rats are, in part, mediated by peripheral opioid receptors.

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In the present study, relationship between each level of PGE, TX B₂ and 6-keto-PGF_1α in the effluent perfusate and vasocontractile response to noradrenaline (NA-R) was examined using the isolated perfused arterial segment of a rabbit ear. The following results were obtained.
1. NA-R was significantly augmented under the conditions infusing either platelet poor plasma (PPP) or platelet rich plasma (PRP), when compared with the control one during perfusion of modified normal Krebs solution (N-R) alone.
2. During PPP infusion, PGE level alone and during PRP infusion, both PGE and TX B₂ levels showed significant increment in comparison with the each control ones during perfusion of N-R, respectively. 6-keto-PGF_1α level was significantly altered under the conditions infusing neither PPP nor PRP.
3. There was the positively significant correlation between ΔNA-R and Δ (TX B₂/PGE ratio), which represent the difference between the control value during perfusion of N-R and the one during infusion of either PPP or PRP, respectively.
From the results obtained, it seems possible to draw the conclusion that the augmen-tation in NA-R induced by PPP or PRP relates, at least in part, to the secondary alteration of PGE and prostanoids metabolism in the arterial preparation.

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