Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01042 (bradykinin)
 15,585 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of various smooth muscle stimulants and relaxants was examined on isolated rabbit trachea and bronchus. Trachea contracted maximally in response to carbachol, slightly to KCl, and there was no response to serotonin or PGF2alpha. Relaxation of carbachol-contracted trachea was elicited by papaverine, aminophylline, isoproterenol, bradykinin, or PGE2. Histamine also relaxed the rabbit trachea. However, bronchi from the same animal contracted to this amine. As was the case with trachea, the bronchi contracted maximally to carbachol and slightly to KCl; serotonin and PGF2alpha were inactive. Unlike trachea, only papaverine or aminophylline completely relaxed the rabbit bronchus. The other relaxants tested produced smaller responses. Contractions induced by carbachol were blocked by atropine. Bronchial contractions caused by histamine were antagonized by pyrilamine. In contrast, relaxation of trachea caused by histamine was neither affected by pyrilamine nor burimamide, metiamide, or propranolol. We conclude that a lack of pharmacological uniformity exists in at least two smooth muscle subdivisions of a mammalian airway and that this must be taken into consideration when determining the action of drugs on the respiratory system.
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PMID:Comparison of drug-induced responses of rabbit trachea and bronchus. 82 43

1. Renal prostaglandins act primarily as local hormones, having their effects at, or near to, sites of synthesis. PGE2 is a major determinant of renal vascular reactivity; it opposes the vasoconstrictor and natriuretic actions of pressor hormones and brakes the release of noradrenaline from adrenergic nerves. In the unanaesthetized rabbit prolonged inhibition of prostaglandin synthesis results in hypertension. In the rat, however, renal prostaglandins augment pressor stimuli. 2. Basal efflux of renal prostaglandins is positively correlated with blood flow to the inner cortex and medulla. Those stimuli which increase renal medullary blood flow do so primarily by activating prostaglandin synthetase. 3. Kinins increase prostaglandin synthesis which action modifies the renal effects of kinins. Thus, one or more renal prostaglandins contribute to the renal vasodilator action of bradykinin and mediate its effect on excretion of water as well as possibly attenuating the natriuretic action of the polypeptide. Kinins in addition to stimulating prostaglandin synthesis may determine the principal product of synthetase by regulating the enzyme PGE 9-ketoreductase, which converts PGE to PGF. The coupling of these systems within the kidney appears unique--prostaglandins mediate some of the actions of kinins and modulate others, whereas they depend on the intrarenal generation of kinins to set their level and type of activity.
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PMID:Renal prostaglandins. 82 36

1 Isolated pulmonary arterial and vein strips from sensitized or non-sensitized chickens exhibited dose-dependent contractions to adrenaline greater than, noradrenaline greater than, 5-hydroxytryptamine greater than, histamine greater than, dopamine. Individual variability in the responsiveness of the vessels to agonists was marked. In general veins were 2 to 25 times more sensitive to agonists than arterial strips. 2 Isoprenaline (a relatively specific beta-adrenoceptor agonist) induced relaxation of the submaximally contracted pulmonary vein and arteries at low doses and contractions at high concentrations. 3 Contractile responses to acetylcholine or carbachol were not regularly recorded; only 50% of the vessels reacted to cholinoceptor agonists over a wide threshold dose range. 4 Chicken pulmonary vessels were found relatively insensitive to bradykinin. 5 Effects of prostaglandins were variable. Prostaglandin F2alpha induced dose-related contractions of the vein and arterial strips; prostglandins E1 and E2 at low doses partially contracted pulmonary artery irrespective of the spasmogen used and further increase in doses induced either no effect or contractions. Prostaglandin E1 induced marked and rapid contractions of the vein. Prostaglandin E2 induced relaxations of the prostaglandin F2alpha-contracted vein only, but produced no effect or slight contractions of the veins partially contracted to other spasmogens. 6 Pulmonary arterial and vein strips obtained from chickens sensitized to horse plasma exhibited Schultz-Dale contractions of variable magnitude and duration to specific antigenic challenge only. In many vessels, antigen-induced contractions were associated with marked increase in spontaneous activity. 7 The importance of the Schultz-Dale reaction in avian pulmonary vessels is discussed in relation to the right heart dilatation associated with anaphylaxis in the chicken.
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PMID:Anaphylactic contraction of pulmonary blood vessels of chicken. 83 99

1 The activity produced by intra-arterial bradykinin and prostaglandin E1 was investigated in multifibre strands dissected from the saphenous nerves of anaesthetized rats. 2 Bradykinin (0.5-10mug) alone produced little activity in nerve strands but produced considerable activity following a 10 min infusion, but not a single injection, of prostaglandin E1 (5-100 ng). 3 Prostaglandin E, alone produced a few large height spikes but following several injections of bradykinin smaller height spikes were also produced by prostaglandin E1. 4 It was concluded that the presence of a low concentration of prostaglandin E, is required for bradykinin to manifest its actions and that bradykinin and prostaglandin E1 are mutually potentiating in their effects on afferent nerve terminals.
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PMID:The effects of bradykinin and prostaglandin E1 on rat cutaneous afferent nerve activity. 83 21

A comprehensive study was undertaken to evaluate the effects of inhibition of prostaglandin (PG) synthesis on a variety of reactions in the coronary vascular bed of anesthetized, open-chest dogs. In 23 dogs an electromagnetic flow probe (EMFP) and hydraulic occluder were placed around either the left anterior descending or circumflex branches of the coronary artery and a needle was inserted distral to the EMFP. Injections into the coronary artery of arachidonic acid (AA), bradykinin, adenosine, angiotensin, and PGE2 were given before and after inhibition of PG synthesis by indomethacin (IND) or meclofenamate (MF). The effects of the inhibitors on reactive hyperemia resulting from 5-, 10-, 15-, and 20-second occlusions and the dilation resulting from 90-second exposure to 8% O2 were also examined. In each experiment, inhibition of PG synthesis was ascertained by the elimination of vasodilation to AA. After administration of IND or MF, while baseline coronary blood flow was slightly reduced, the total increment of blood flow to vasodilator agents was not significantly altered. Whereas the peak dilation and volume of reactive hyperemia were decreased, the percent flow debt repaid was unchanged and total increment of coronary flow due to hypoxia-induced vasodilation was not significantly modified. Vasoconstrictor responses to angiotensin were also unchanged. These results indicate that while inhibitors of PG synthesis increase coronary resistance, they do not adversely affect vascular responsiveness. We conclude that prostaglandins play little, if any, role in modulating coronary blood flow.
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PMID:Prostaglandins and the control of blood flow in the canine myocardium. 83 79

Generation of a prostaglandin of the F series by bovine mesenteric veins in response to bradykinin may depend on increased synthesis of PGE and conversion of the latter to PGF after activation of PGE 9-ketoreductase by the kinin. The prostaglandin then mediates the constrictor action of bradykinin on the bovine mesenteric vein. A high speed supernatant (HSS) fraction of bovine mesenteric blood vessels contains the highest activity of PGE 9-ketoreductase. Incubation of PGE2 with HSS at 37 degrees C in the presence of a NADPH generating system resulted in time-dependent conversion of PGE2 to PGF2alpha. Bradykin (0.01mM) more than doubled conversion of PGE2 to PGF2alpha by the PGE 9-ketoreductase obtained from mesenteric veins whereas the kinin had little effect on enzymic activity of the HSS fraction of mesenteric arteries. However, after inhibition of kininase catabolism, bradykinin increased PGE 9-ketoreductase activity of arteries and veins to the same degree. Prostaglandin release from veins by bradykinin appears essential to contraction of mesenteric venous strips evoked by the polypeptide as indomethacin treatment abolished this effect. PGE 9-ketoreductase may be an important prostaglandin regulatory mechanism of the vascular wall whereby the functional consequences of changes in rates of prostaglandin synthesis are governed by determining the ratio of PGE to PGF within vascular tissue. Constriction of bovine mesenteric veins evoked by bradykinin may, therefore, depend on increased prostaglandin synthesis and conversion of newly formed PGE to PGF, both steps being affected by the kinin.
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PMID:Dual effects of bradykinin on prostaglandin metabolism: relationship to the dissimilar vascular actions of kinins. 88

Indomethacin had an equal inhibitory effect on the response of the guinea-pig isolated ileum to angiotensin II (angiotensin), bradykinin, histamine and acetylcholine. This effect did not seem to result from inhibition of prostaglandin synthesis, as it did not depend on the time of treatment with indomethacin. Prostaglandin E2 (prostaglandin) potentiated the responses of the guinea-pig ileum to angiotensin, bradykinin, histamine and acetylcholine without significant differences in the effects observed. In the rabbit isolated mesenteric and coeliac arteries, indomethacin had an equal potentiating effect on the responses to angiotensin and to adrenaline. In these organs pre-incubation with indomethacin was necessary for the effect to be observed, and this effect lasted for 2 h or more after that drug was removed from the medium. No cross-tachyphylaxis between angiotensin and adrenaline was observed in the rabbit mesenteric and coeliac arteries. It is concluded that the effects of indomethacin and prostaglandin on the response of the guinea-pig ileum to the four agonists result from an action on the smooth muscle contractile mechanism per se rather than from an inhibitory action on the release of endogenous prostaglandin produced by the four agonists. The results with the rabbit isolated arteries indicate that tachyphylaxis to angiotensin in these organs is not caused by prostaglandin release.
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PMID:Effect of indomethacin and prostaglandin on the smooth muscle contracting activity of angiotensin and other agonists. 97 84

E-type PGs, injected in rat skin at a low dose concentration (1-5 ng ml-) proved not to release vasoactive amines from local mast cell, enhance increase in vascular permeability evoked by hypersensitivity endogenous inflammatory reactions (passive cutaneous anaphylaxis and reversed passive Arthus) or by intradermal injection of histamine and bradykinin. The possible role of PGE1 and PGE2 as modulators of the inflammatory response is discussed.
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PMID:Prostaglandins as modulators of the inflammatory response in the rat. 102 39

The activity of prostaglandins (PG) in producing vascular permeability was quantitated by dye extraction method in skin of anaesthetized rabbits. PGE1 and PGE2 (0.01-10 mug) produced increase in vascular permeability. Activity was approximately equal to that of histamine (Hist) and 1/20 of that of bradykinin (BK) on a weight basis. The activity of PGF1alpha and PGF2alpha was only 1/20 of that of PGE1 or PGE2. In spite of the relatively low potency of PGE1 and PGE2 in the rabbit, near threshold doses (0.1 or 1 mug) of PGE2 could potentiate permeability responses to bradykinin (0.1 mug) by 10 or 100-fold, respectively. Equivalent doses (0.1 or 1 mug) of histamine could not potentiate the bradykinin responses. Arachidonic acid (AA) at 1 mug, produced a 10-fold potentiation in the permeability response to bradykinin (0.1 mug). Pretreatment of the rabbits with indomethacin (20 mg/kg, i.p.) reduced the responses of BK (0.1 mug) + AA (1 mug) down to a similar magnitude of those seen with bradykinin alone. However, indomethacin did not block responses to either, BK alone, BK + PGE2, or BK + Hist. Various doses (1, 10, 100 and 300 mug) of arachidonic acid alone also produced increase in cutaneous vascular permeability, although its potency was only 1/3-1/8 of that of PGE2. This activity of arachidonic acid was attributed in part to its bioconversion to PGE2, since its activity was significantly reduced by the prostaglandin antagonist, diphloretin phosphate (DPP) (60 mg/kg, i.v.) and by indomethacin (20 mg/kg, i.p.), which blocks conversion of arachidonic acid to prostaglandins. Arachidonic acid may owe some of its permeability increasing effects to histamine release, since its effects were also reduced by the anti-histamine, pyrilamine (2.5 mg/kg, i.v.).
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PMID:Potentiation of bradykinin-induced vascular permeability increase by prostaglandin E2 and arachidonic acid in rabbit skin. 121 37

1 Intradermal injection of prostaglandin (PG) D1 and D2 in the human forearm produced a long-lasting dose-related erythema. When compared with prostaglandin E1 or E2 the order of potency for erythema production was PGE1 greater than PGE2 greater than PGD2 greater than PGD1. 2 In rat skin, prostaglandin D2 but not D1 caused an increase in vascular permeability as quantitated by the Evans blue method and the 125I-albumin extravasation technique. Prostaglandin E2 was 3-5 times more potent than prostaglandin D2. 3 Prostaglandin D2 (10 ng) potentiated the increase in vascular permeability in rat skin produced by histamine, but not that produced by bradykinin. 4 Prostaglandin D2 (10, 20 and 50 ng) did not elicit oedema or hyperalgesia in the rat paw oedema test, but potentiated carrageenan-induced oedema; hyperalgesia was potentiated by doses of 100 ng and above.
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PMID:Inflammatory effects of prostaglandin D2 in rat and human skin. 125 71


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