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Biomedical subjects

R Inoki

Publications and source records attributed to R Inoki.

At least 73 records · Page 4Linked to original sources
PubMed1984

Effects of morphine and (D-Ala, Met)-enkephalinamide on 45Ca-uptake to rat brain striatal slices.

Effects of morphine and (D-Ala, Met)-enkephalinamide on 45Ca-uptake to rat striatal slices were examined. While morphine didn't give any effect on 45Ca-uptake to striatal slices in normal Krebs-Ringer solution, it inhibited K+ (40 mM)-stimulated 45Ca-uptake to slices. In high K+ medium, 45Ca-uptake was enhanced to 170% and this was reduced to 147 and 137% by 10(-5) and 10(-4) M morphine, respectively. Furthermore, the effect of morphine was antagonized by 10(-5) M naloxone. (D-Ala, Met)-enkephalinamide (10(-4) M) also inhibited K+-stimulated 45Ca-uptake to the slices to the same extent as was observed by morphine. K+-stimulated 45Ca-uptake to striatal slices obtained from chronically morphine administered rat (6 mg/kg, twice/day, 7 days) was not inhibited by morphine.

Animals↗
PubMed1984

Effect of neuroactive peptides on labeled 5-hydroxytryptamine release from rat spinal slices in vitro.

Effects of neuroactive peptides on the release of labeled 5-hydroxytryptamine (5-HT) from preloaded rat spinal cord slices were investigated. The 5-HT release was significantly stimulated by somatostatin (10-50 microM) and substance P (10-50 microM), but not by neurotensin (50 microM), beta-endorphin (30 microM) and methionine-enkephalin (met-enk) (100 microM). Somatostatin-stimulated 5-HT release was markedly inhibited by gamma-aminobutyric acid (GABA) (30 microM), but not by baclofen (30 microM) and met-enk (100 microM). Substance P-stimulated 5-HT release was strongly inhibited by GABA (30 microM) and baclofen (30 microM), but not by met-enk (100 microM). High concentrations (20 mM) of potassium also stimulated 5-HT release. The high potassium-stimulated 5-HT release was not affected by GABA (30 microM) and met-enk (100 microM). These results suggested further evidence on the important role of somatostatin and substance P as modulators of serotonergic neurones.

Animals↗
PubMed1983

Effect of inhalational anesthetics on the opioid receptors in the rat brain.

Effects of inhalational anesthetics, methoxyflurane and halothane, on the binding of various opioid ligands were studied. The binding affinity of 3H-methionine enkephalin (delta) was reduced by both anesthetics in the same manner, but the receptor density was not significantly affected. Methoxyflurane decreased the binding affinity but increased the receptor density of 3H-dihydromorphine (mu), while halothane had little effects on both affinity and density. Methoxyflurane also decreased binding affinities of 3H-ethylketocyclazocine (kappa) and 3H-SKF-10047 (sigma), but halothane did not decrease significantly. These effects of the anesthetics were completely disappeared by unsealing and ventilation.

Animals↗
PubMed1983

Changes of the Met-enkephalin-like peptide content induced by noxious stimuli in the rat incisor pulp.

It was examined what mechanism involved in an increase of met-enkephalin (met-EK)-like peptide content in the pulp induced by noxious stimuli. The increased content of the peptides by cavity formation as noxious stimulation was not influenced by cycloheximide, but attenuated by FOY-305 [N,N-dimethyl carbamoyl-methyl 4-(4-guanidinobenzoyloxy) phenyl acetate methanesulfonate], a trypsin-like enzyme inhibitor, and enhanced by captopril, and attenuated by infusion of saline in the pulp cavity. From these results, it was suggested that noxious stimuli on the pulp led to activation of trypsin-like enzymes followed by an increased content of met-EK-like peptides, and thereafter, the peptides, such as met-EK, might be degraded by angiotensin converting enzyme (ACE). Furthermore, an immunohistochemical study demonstrated that met-EK-like immunoreactivity (met-EK-IR) of cells in the rat incisor pulp was clearly increased following tryptic digestion of the pulp section, supporting a suggestion mentioned above.

Animals↗
PubMed1983

A possible relationship between processing from precursor proteins to opioid peptides and noxious stimulation in the rat incisor pulp.

The content of met-enkephalin (met-EK)-like peptides in a crude extract from intact pulp of the rat markedly increased with tryptic digestion but not with carboxypeptidase B(CPase B) digestion, while the content of leu-enkephalin (leu-EK)-like peptides more markedly with CPase B- than with tryptic digestion. On the other hand, results by High Performance Liquid Chromatography (HPLC) showed that the contents of both met-EK-Arg-Phe and leu-EK in cavity formed pulp increased 6 times as much as those contents in intact pulp, while the met-EK content in cavity formed pulp increased 2 times as much as that in intact pulp. Furthermore, results by gel filtration of crude extract from intact pulp showed that one peak of met-EK-like immunoreactivity (met-EK-IR) appeared at position of approximately 30,000 of molecular weight and a broad peak of leu-EK-IR appeared at position of approximately 60,000 of molecular weight following tryptic digestion. From these results, it was suggested that noxious stimuli might cause activation of trypsin-like enzymes followed by processing from one precursor protein to met-EK-like peptides as well as from another to leu-EK-like peptides in the rat incisor pulps.

Animals↗
PubMed1981

Algesiogenic and analgesic activities of synthetic substance P.

The objective of our study was to determine whether the pure synthetic substance P(SP) is algesiogenic or analgesic when administered centrally or peripherally. The relationships between SP-induced analgesia and the content of morphine-like factor (MLF) in the brain were also studied. Intracarotid arterial administration of SP (20-200 microgram) produced no pseudoaffective responses to pain in six out of nine rats, but in the remaining three, there was an exhibition of these responses. Chlorpheniramine pretreatment antagonized these responses. On cantharidin blister base experiments in humans, SP (10(-3) g/ml) produced slight pain and an itchy sensation. SP given intracerebroventricularly produced an analgesia in mice in a dose of 5 ng/mouse, as determined by the acetic acid-induced writhing and hot plate methods. These SP-induced analgesia were antagonized by naloxone pretreatment. SP did not alter the content of MLF in the mouse whole brain. However, SP5-11 not only produced an analgesia but also increased the content of MLF. These results suggest that SP has a slight algesiogenic activity which might be mediated by histamine and a slight analgesic activity which might be mediated by MLF.

Analgesics↗
PubMed1980

Inhibitory action of morphine on the release of a bradykinin-like substance after sciatic nerve stimulation.

Effects of morphine on the release of a bradykinin-like substance into the subcutaneous perfusate of the rat paw, elicited by pinching and heating of the foot instep and by electrical stimulation of the sciatic nerve, were investigated. Morphine (5 mg/kg i.m.) inhibited the release of a bradykinin-like substance only when sciatic nerve stimulation was applied. The release due to sciatic nerve stimulation was not inhibited by gallamine (8 mg/kg i.p.), but significantly by physostigmine (1 mg/kg i.p.). The release was also observed by adrenergic agents and was inhibited by adrenergic alpha-blocking agents. No release of a bradykinin-like substance due to sciatic nerve stimulation was observed in reserpinized and 6-hydroxydopaminized rats. Dopa restored the releasing ability due to sciatic nerve stimulation in the reserpinized rats, but not in the 6-hydroxydopaminized ones. The results suggest that the inhibitory action of morphine can be explained by an inhibition of the release of noradrenaline.

Animals↗
PubMed1979

Significance of adrenergic alpha-effect on salivary kallikrein secretion in the submandibular gland of the dog.

The effects of the sympathetic nerve stimulation and the administrations of sympathomimetics on the secretion of salivary kallikrein induced by the chorda tympani stimulation were examined quantitatively and qualitatively in the submandibular gland of the dog. The secretion of salivary kallikrein may be mediated through both adrenergic alpha- and beta-receptors. The activities of salivary kallikrein secreted by either the chorda tympani stimulation or isoproterenol were not inhibited by soy bean trypsin inhibitor in vitro, but those secreted by the sympathetic nerve stimulation and noradrenaline or adrenaline were markedly inhibited in vitro. These results suggested that secretion of glandular kallikrein was induced by the chorda tympani stimulation and the sympathetic beta-stimulation, and secretion of plasma kallikrein was induced by the sympathetic alpha-stimulation.

Animals↗
PubMed1979

Bradykinin as an algesic (pain producing) substance in the pulp.

A rat uterine smooth muscle contracting substance was released into the superfusate of the dog's exposed canine pulp after noxious stimulation of the pulp by pricking, heat and electrical stimulation. This active substance was acid- and heat-resistant and was decomposed by carboxypeptidase B and alpha-chymotrypsin, but not by carboxypeptidase A and trypsin. This substance was also tested on several types of smooth muscle. Electrical activity of nerve cells in the reticular formation, which were sensitive to stimulation of the instep of the foot by pinching, was activated by the intrafemoral administration of the active substance. The algesic activity of this substance was examined in cantharidin blister base in man. This study conclusively demonstrated that the active substance of the pulp released by noxious stimulation produced pain and it was identified as bradykinin.

Animals↗