Effects of morphine on the level of the free fatty acids in the serum of rats.
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Biomedical subjects
Publications and source records attributed to T Muraki.
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Subcutaneous administration of the enkephalin analogue FK33-824 (FK) elicited a dose-related decrease in rectal temperature and respiratory rate in male ddY strain mice. Naloxone and 3 days' implantation of morphine pellet decreased the effects of FK, suggesting the involvement of opioid receptors and cross-tolerance with morphine to both effects of FK. A positive correlation was found between the FK-induced decrease in rectal temperature and that in respiratory rate among the 6 strains of inbred mice including BALB/c, C3H, A/J, CBA, C57BL/6 and DBA/2. The degree of hypothermia elicited by FK was different among strains, whereas marginal strain difference was seen in the respiratory depression induced by FK. The strain difference in the FK responses may be due to the difference in the opioid receptor subtypes in the brain.
Effects of bombesin on brown adipose tissue (BAT) thyroxine (T4) 5'-deiodinase (5'D) activity and rectal temperature were examined in male mice. Immediately following an intracerebroventricular (ICV) or intravenous (IV) injection of bombesin (0.1-100 ng/animal) or vehicle (20 mM bacitracin dissolved in 0.9% saline), the mice were placed in a room at 4 degrees C or 22 degrees C for 30, 60, 120 or 240 min. The ICV injection of bombesin dose-dependently lessened cold-induced increase in BAT 5'D activity and increased hypothermia determined at 120 min of cold exposure, whereas the IV injection of bombesin was without effect. Bombesin (ICV)-induced hypothermia preceded the inhibition of BAT 5'D activity by at least 30 min at 4 degrees C. BAT 5'D activity was not affected by ICV injection of bombesin in mice kept at 22 degrees C, although the rectal temperature was significantly decreased. Bombesin thus appears to prevent cold-induced increase in T4 5'D activity in mouse BAT by its central effect. Bombesin-induced excessive hypothermia itself and/or the decrease in sympathetic tone of BAT by bombesin might decrease cold-induced increase in BAT 5'D activity.
The response of isolated duodenum to neuropeptide Y (NPY) was studied isotonically in neonatal and adult rats. Neuropeptide Y (10(-8) to 10(-6) M) elicited a biphasic contraction of isolated duodenum from neonatal rats, but monophasic and weak contraction of adult duodenum. The first phase of NPY-induced contraction of neonatal duodenum was concentration dependent and partially inhibited by preincubation with tetrodotoxin, a Na+ channel blocker, hyoscine, a muscarinic antagonist, suramin, a P2 purinoceptor antagonist, and indomethacin, an inhibitor for prostaglandin biosynthesis. Neuropeptide Y(13-36), a specific Y2 NPY receptor agonist, elicited a concentration-dependent contraction of neonatal rat duodenum. The duodenal response to NPY thus changes during development in rats. Both cholinergic and purinergic transmission and prostaglandin biosynthesis may be involved in the NPY-induced contraction of neonatal duodenum. Neuropeptide Y-induced contraction may be mediated through presynaptic Y2 receptors.
Using mouse thyroid lobes incubated in vitro, a study was made of the subtype of alpha-adrenoceptors involved in iodide organification, induced by norepinephrine, and the possible role of protein kinase C in mediating the effect of norepinephrine. Norepinephrine and phenylephrine, alpha 1-agonists, increased the iodide organification in mouse thyroid lobes; however, clonidine, and alpha 2-agonist, showed a marginal effect. Prazosin, an alpha 1-blocker, but not yohimbine, an alpha 2-blocker, inhibited the norepinephrine-induced iodide organification. These results suggest the involvement of alpha 1-adrenoceptors. The stimulation of the iodide organification, induced by norepinephrine, was inhibited by omission of calcium from the medium and by protein kinase C inhibitors such as H 7, quercetin and trifluoperazine, but not by W-7, a calmodulin antagonist. Since tetradecanoylphorbol acetate, a stimulator of protein kinase C, mimicked the effect of norepinephrine in increasing iodide organification, extracellular calcium ion and protein kinase C would appear essential to the alpha 1-adrenergically regulated iodide organification in mouse thyroid.