UMLS:C0011570 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In order to determine the nervous outflow from skeletal muscle during chemically induced muscle pain, the impulse activity of various types of muscle afferents in response to close intra-arterial injections of pain-producing substances (bradykinin, 5-hydroxytryptamine, histamine and potassium) was studied in anaesthetized cats using a single fibre recording technique.2. By administration of algesic agents in doses which produce pain in man and pain reactions in animals, about half of the group IV and two thirds of the group III muscle afferents could be activated. In contrast, group II and group I afferent units were usually not excited by chemical noxious stimulation. If effects at all occurred in the thick myelinated afferents, they consisted of a depression of the fibre activity rather than of an activation.3. The qualitative features of the discharges of group III muscle afferents induced by chemical stimulation resembled those of the group IV units very closely. The group III units differed from the group IV afferents in that their responses to a given dose of bradykinin were of greater magnitude.4. It is concluded that the chemically induced muscle pain is probably mediated by certain portions of the group IV and group III afferents, whereas the reactions of group II and group I units to algesic agents are such that a contribution to muscular chemo-nociception seems improbable.
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PMID:Nervous outflow from skeletal muscle following chemical noxious stimulation. 14 96

Intravenous baclofen (1 mg/kg) abolished or severely attenuated the high threshold late component (but not the low threshold early component of long duration (greater than 150 msec) discharges evoked in cat dorsal horn neurons by intense transcutaneous electrical stimulation. Baclofen similarly reduced the spontaneous activities and discharges evoked by intra-arterial bradykinin in these same cells. These powerful inhibitions of dorsal horn interneurons may be the basis of baclofen's reported analgesic actions and could contribute to depression in reflex excitability of motoneurons.
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PMID:Effects of intravenous baclofen on dorsal horn neurons of spinal cats. 21

Although the pigment leakage method is one of the most conventional for determining vascular permeability, accuracy in macroscopic measurement of the diameter of the stained area with an arbitary scale leaves much to be desired. We developed a simple and beneficial method for quantitative assay using a densitometer (Chromatoscanner CS-900). Guinea pigs weighing 300 approximately 350 g were used. Formalin as a phlogistic, in a dose of 2.3 approximately 37 mg was injected intradermally in the shaved skin of the back, and 15 mg/kg of pontamine blue was then given into the femoral vein. One hour after the injection the animals were sacrificed and the skin of the back, which was stained by the leaked pigment, was stripped off and allowed to adhere to a wooden plate for 24 hours. Reflection and a zig-zag scanning technique were used to measure the volume of the leaked pigment. There was a liner relationship between the dose of formalin and the integrated values. A dose-dependent relationship was also obtained when histamine, serotonin, kallikrein and bradykinin were used as phlogistics. Representative anti-inflammatory drugs such as aspirin, hydrocortisone, oxyphenbutazone, benzydamine, diclofenac sodium, sodium salicylate and aminopyrine depressed the leakage due to formalin. Depression of leakage by aspirin in a dose of 400 mg/kg was the most remarkable. Pigment leakage elicited by histamine, serotonin, kallikrein and bradykinin was examined on the same individual animal. Aspirin more than the other agents depressed the leakages due to bradykinin and kallikrein. Hydrocortisone and oxyphenbutazone depressed the leakage due to bradykinin, serotonin and histamine, but enhanced that due to kallikrein. The results obtained were consistent with those of a previous study and as this method is simple and more reliable, it is applicable for assay of anti-inflammatory compounds.
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PMID:[A new method for assaying anti-inflammatory drugs. Quantitative analysis of pigment leakage into skin by Chromatoscanner CS-900 (author's transl)]. 56 14

Effects of beta-(p-chlorophenyl)-GABA (baclofen), a muscle relaxant, on the response of mice and rats to various noxious stimuli were studied. In mice, 5 approximately 10 mg/kg i.p. of baclofen delayed the response time to tail-pinch and hot-plate stimuli but the relaxation was also apparent with this dose range. Mephenesin also delayed the response time to tail-pinch stimuli with the dose producing muscle relaxation. Baclofen, 3 mg/kg i.p., while producing no muscle relaxation, suppressed the acetic acid-induced writhing. The same effect, suppression of writhing and no muscle relaxation, was achieved with 50 mg/kg i.p. of mephenesin. In rats, baclofen (5 approximately 10 mg/kg i.p.) increased the response threshold in Randall-Selitto method and suppressed the bradykinin-induced symptoms, however, muscle relaxation was also produced with these same doses. Increase in response threshold in Randall-Selitto method was achieved with the dose of mephenesin producing muscle relaxation. The time courses of the depression of response to noxious stimuli and the muscle relaxation induced by baclofen and mephenesin were consistent in mice and rats. A small dose (3 mg/kg i.p. in mice, 2 mg/kg/h s.c. in rats) of baclofen reduced the antinociceptive effect of morphine but a larger dose (5 mg/kg i.p. in mice, 7 mg/kg/h s.c. in rats) of baclofen increased or did not alter the effect of morphine. It seems likely that the antinociceptive effect of baclofen may be nonspecific to analgesia.
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PMID:[Effects of beta-(p-chlorophenyl)-GABA (baclofen) on response to noxious stimuli (author's transl)]. 59 82

In order to complete previous results of the efficacy of the horse chestnut saponin escin, its activity was tested on two further models of inflammation: the rat serous peritonitis provoked by i.p. injection of formalin solution, and the rat serous pleurisy provoked by intrapleural injection of Evans Blue/carrageenan. The results showed escin to be an anti-exudative substance with regard to its exudation inhibitory effect determined by the reduction of exudative fluid. As to peritonitis the diminution of protein permeation into the abdominal cavity was determined: with increasing doses escin tended to prevent more efficiently the diffusion of small molecules than the permeation of large molecules. The hypothesis that escin has an effect on the vascular walls in the sense of a "sealing" effect on the capillaries was tested on the following model: the permeability of the plasma-lymph barrier of the hind leg of the rabbit was enhanced by injection of bradykinin. Escin antagonised the bradykinin effect dose-dependently determined by the depression of the raised lymph-flow by about 70%.
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PMID:[New findings on the efficacy and mode of action of the horse chestnut saponin escin]. 94 3

In experiments on the isolated strips of Taenia coli of guinea pigs it was shown that compound D-600 depressed the acetylcholine (5-10(-6), histamine (2-10(-6) and bradykinin (10(-5) gl/ml)-induced contractile response of depolarized smooth muscle. Along with depression of the drug-induced response, compound D-600 depressed the "potassium contracture". It is supposed that the mentioned agents activated the inward flow of Ca2+ ions through the membrane, but not the release of these ions from the sarcoplasmic reticulum.
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PMID:[The effect of biologically active substances (acetylcholine, histamine and bradykinin) on depolarization of taenia coli smooth muscle]. 124 65

Studies of regional cerebral blood flow in migraine with aura have shown that the aura phase is associated with hypoperfusion in the cortical area which relates topographically to the clinical symptoms. Thus, the previously hypoperfused area becomes hyperperfused. However, there is no strict association between hyperperfusion and headache. The mode of hypoperfusion propagation recalls the circulatory manifestations of experimental cortical spreading depression. In addition, there are no focal cerebral blood flow abnormalities in migraine without aura. During the headache phase of migraine, dilation of both the large extra- and intracranial arteries takes place. A bulk of biochemical evidence has suggested that the pain in migraine is caused by blood vessels which are dilated and sensitized by circulating pain-producing substances e.g. bradykinin, serotonin and histamine (sterile inflammation). Recently, perivascular trigeminal fibres (trigeminovascular system) which, when stimulated, release sensory peptides (substance P and the calcitonin gene-related peptide) capable of provoking marked vasodilation and plasma extravasation (neurogenic inflammation) have been identified. Thus, the activation of the trigeminovascular system is probably involved in the vasodilatative and nociceptive phenomena of the migraine attack. The finding of a reduced endorphinergic brain tonus in migraine patients supports the hypothesis of a central nociceptive derangement in migraine. Nonetheless, the exact relationship between vasodilation and headache remains to be defined. However, the potent antimigraine effectiveness of sumatriptan--an agonist of the serotonin receptors which selectively constricts dilated arteries during the migraine attack--once again stresses the fact that serotonin is probably the crucial factor in the link between vasodilation and headache.
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PMID:[The pathogenetic bases of hemicrania]. 129 98

This study examines the action of three putative functional bradykinin (BK) antagonists isolated from Mandevilla velutina on BK and other agonist-induced contraction or relaxation responses in intact or in epithelium-denuded strips of tracheal muscle from guinea pigs. Compound MV 8612 (8 and 16 microM) and MV 8610 (12 and 24 microM) caused a graded rightward displacement of BK dose-response curves in the isolated guinea pig trachea (dose ratio 2- to 4-fold). Compound MV 8608 (28 microM) had a small effect on BK contractile responses. At high concentrations, compound MV 8612 (24 microM) caused a slight but significant depression of the BK-induced maximal responses. These pharmacological actions appear to be quite selective towards BK, since within the same concentration range these compounds failed to interfere with the sensitivities to prostaglandin F2 alpha, carbachol and histamine. However, these compounds significantly enhanced maximal responses to the latter two agonists, an action that was not influenced by indomethacin. In addition, MV 8612 and MV 8608 (16 and 56 microM) significantly potentiated BK-mediated epithelium-dependent relaxation responses in preparations precontracted with carbachol. These compounds also significantly potentiated isoprenaline but not theophylline-relaxant responses, an action that seems to occur independently of the generation of cyclooxygenase products of arachidonic acid pathway. These results further extend our previous studies and indicate that some of the M. velutina compounds exert a weak though selective antagonistic action against BK-induced contractile responses of the isolated epithelium-denuded guinea pig tracheal smooth muscle and potentiate BK-induced relaxations in tissues with intact epithelium precontracted with carbachol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of compounds from Mandevilla velutina on bradykinin-mediated contractile and relaxant responses of the isolated guinea pig trachea. 138 76

In order to extend the in vivo pharmacological profile of CP-96,345 ((2S,3S)-cis-2-(diphenylmethyl)-N-((2-methoxyphenyl)- methyl)-1-azabicyclo[2.2.2]octan-3-amine dihydrochloride), a non-peptide antagonist of substance P, the compound was tested against substance P-induced effects on blood pressure in rabbits and on respiration pressure in guinea-pigs. In addition, CP-96,345, and its inactive (2R,3R)-enantiomer, CP-96,344, were also tested in 2 models involving presumably substance P-mediated reflexes in the rat. The fall in blood pressure evoked by i.v. injections of substance P in the rabbit was inhibited by 0.3 mumol kg-1 CP-96,345 i.v. for at least 30 min, and almost abolished, for at least 2 h, by 3 mumol kg-1. In guinea-pigs, the bronchoconstriction induced by i.v. injections of substance P, but not that in response to histamine or bradykinin, was inhibited by CP-96,345 (0.6 and 6.0 mumol kg-1, i.v.) in a dose-dependent manner and this inhibition lasted for 40 min and 70 min, respectively. CP-96,345 (3-20 mumol kg-1, i.v.) reduced depressor reflexes in response to stimulation of peripheral capsaicin-sensitive neurones in the rat. However, the inhibition was not dose-dependent and was also seen with the inactive enantiomer, CP-96,344. This effect can hardly be attributed to receptor-specific effects of CP-96,345 and may be related to unspecific actions such as those involved in the cardiac depression exhibited by both enantiomers. The present results show that CP-96,345 is a potent antagonist of substance P in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:CP-96,345, a non-peptide antagonist of substance P: II. Actions on substance P-induced hypotension and bronchoconstriction, and on depressor reflexes in mammals. 138 35

1. The M-like current IK(M,ng) in differentiated NG108-15 mouse neuroblastoma x rat glioma hybrid cells has been studied using tight-seal, whole-cell patch-clamp recording. 2. When calculated from steady-state current-voltage curves, the conductance underlying IK(M,ng) showed a Boltzmann dependence on voltage with half-activation voltage Vo = -44 mV (in 3 mM [K+]) and slope factor (a) = 8.1 mV/e-fold increase in conductance. In 12 mM [K+] Vo = -38 mV and a = 6.9 mV. The deactivation reciprocal time constant accelerated with hyperpolarization with slope factor 17 mV/e-fold voltage change. 3. The reversal potential for deactivation tail currents varied with external [K+] as if PNa/PK were 0.005. 4. Steady-state current was increased on removing external Ca2+. In the presence of external Ca2+, reactivation of IK(M, ng) after a hyperpolarizing step was delayed. This delay was preceded by an inward Ca2+ current, and coincided with an increase in intracellular [Ca2+] as measured with Indo-1 fluorescence. Elevation of intracellular [Ca2+] with caffeine also reduced IK(M, ng). 5. IK(M, ng) was inhibited by external divalent cations in decreasing order of potency (mM IC50 in parentheses): Zn2+ (0.011) greater than Cu2+ (0.018) greater than Cd2+ (0.070) greater than Ni2+ (0.44) greater than Ba2+ (0.47) greater than Fe2+ (0.69) greater than Mn2+ (0.86) greater than Co2+ (0.92) greater than Ca2+ (5.6) greater than Mg2+ (16) greater than Sr2+ (33). This was not secondary to inhibition of ICa since: (i) inhibition persisted in Ca(2+)-free solution; (ii) La3+ did not inhibit IK(M, ng) at concentrations which inhibited ICa; and (iii) organic Ca2+ channel blockers were ineffective. Inhibition comprised both depression of the maximum conductance and a positive shift of the activation curve. Addition of Ca2+ (10 microM free [Ca2+]) or Ba2+ (1 mM total [Ba2+]) to the pipette solution did not significantly change IK(M, ng). 6. IK(M, ng) was reduced by 9-amino-1,2,3,4-tetrahydroacridine (IC50 8 microM) and quinine (30 microM) but was insensitive to tetraethylammonium (IC50 greater than 30 mM), 4-aminopyridine (greater than 10 mM), apamin (greater than 3 microM) or dendrotoxin (greater than 100 nM). 7. IK(M, ng) was inhibited by bradykinin (1-10 microM) or angiotensin II (1-10 microM), but not by the following other receptor agonists: acetylcholine (10 mM), muscarine (10 microM), noradrenaline (100 microM), adrenaline (100 microM), dopamine (100 microM), histamine (100 microM), 5-hydroxytryptamine (10 microM), Met-enkephalin (1 microM), glycine (100 microM), gamma-aminobutyric acid (100 microM) or baclofen (500 microM).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Kinetic and pharmacological properties of the M-current in rodent neuroblastoma x glioma hybrid cells. 140 9

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