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)

Adult dogs were sensitized to horse plasma. Reactivity of isolated bronchus and pulmonary blood vessels to antigen and some selected autonomic and autacoid agents were studied. Pulmonary veins contracted to bradykinin, 5-HT, PGF2alpha, PGE2, histamine, carbachol and antigen (Schultz-Dale reaction). Pulmonary arterial strips contracted to 5-HT and histamine, but only weakly to horse plasma. Bronchial strips contracted to carbachol, 5-HT, histamine and horse plasma, relaxed to isoprenaline, PGE1 and PGE2. Subsequent antigen challenge produced 'desensitization'. Allowing the tissues to 'rest' for 1 and 2 h resulted in partial 'recovery' of the anaphylactic response. This investigation suggests that the contractions of sensitized pulmonary vein and bronchus to specific antigen may contribute to the patho-physiology of pulmonary hypersensitivity in dogs.
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PMID:Reactivity of isolated canine bronchus and pulmonary blood vessels to autonomic, autacoid agents and antigen. 3 24

PRD-92-Ea [5,5-Dimethyl-11-oxo-5H, 11H-(2) benzopyrano (4,3-g) (1) benzopyran-9-carboxylic acid ethanolamine], was an active antiallergic compound in rat and monkey experimental models of immediate hypersensitivity. It inhibited, in a dose-dependent manner, the rat PCA reaction after both intravenous and oral administration. It also inhibited the degranulation of rat peritoneal mast cells after antigenic challenge. PRD-92-Ea was also active in preventing bronchoconstriction in Ascaris-sensitive Rhesus monkeys after intravenous, topical and oral administration. Using chopped monkey tissues, it was found that PRD-92-Ea prevented histamine release from the respiratory mast cells, but not from the cutaneous mast cells. No reason for this dichotomy of effect is known. PRD-92-Ea showed antagonistic activity against the allergic mediators released from mast cells. In order of decreasing potency it was active against SRS-A (monkey lung), PGF2alpha, PGE2, serotonin, bradykinin and histamine. Apart from its antiallergic effects PRD-92-Ea had no other significant pharmacological activity.
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PMID:Pharmacologic profile of a new antiallergic compound PRD-92-Ea. 7 14

The bioconversion of tritiated arachidonic acid by microsomal fractions from rat uterus and duodenum is described. In rat duodenum the formation of both prostaglandin E2 and F2alpha is enhanced by the peptide hormone bradykinin. In contrast, bradykinin inhibits the synthesis of PGE2 in rat uterus.
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PMID:Effect of bradykinin on prostaglandin synthetase activity in microsomal fractions from rat duodenum and uterus. 10 27

Renomedullary tissue from rabbit or rat was incubated with angiotensin I, II, III, arachidonic acid, bradykinin, indomethacin and meclofenamate to study their effect on PGE2 production. Arachidonic acid and bradykinin enhanced PGE2 production significantly. Indomethacin and meclofenamate inhibited PGE2 production by more than 70%. Angiotensin I, II and III did not influence PGE2 production. These results suggest that bradykinin and arachidonic acid stimulate PGE2 production by a direct cellular action whereas the angiotensins do not.
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PMID:Influence of angiotensins (I, II, & III), bradykinin and arachidonic acid on renomedullary PGE production in vitro. 11 7

Blood flow and motility were studied in a canine jejunal loop in situ with intact innervation. Bradykinin was administered into a side branch of the supplying artery and indomethacin was infused intravenously 1 h before experiments. In the control group without indomethacin infusion, bradykinin 1-10 nmol/l gradually increased blood flow without significantly altering motility. Higher concentrations of bradykinin (20-100 nmol/l) augmented rhythmic contractions of the intestine. Phasic blood flow decreased during contraction and increased after relaxation, and mean blood flow increased. Bradykinin (0.2-1.0 mumol/l) caused tonic intestinal contractions. Blood flow initially increased but was soon impeded in proportion to the amplitude and duration of the tonic contractions. With intestinal muscle relaxation, blood flow increased to values markedly higher than control. In the group pretreated with indomethacin, blood flow did not increase after bradykinin administration. However, administration of PGE2 produced significant increase in flow, similar to that observed after bradykinin. Acetylcholine or isoprenaline also markedly increased blood flow. Increased intestinal motility caused by bradykinin mechanically impeded blood flow through the intestine, thus masking its direct vasodilating action. The action of bradykinin on the intestinal vascular bed is probably mediated or modulated by endogenous prostaglandin-like substances.
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PMID:On the contribution of prostaglandin-like substances to the action of bradykinin on intestinal motility and blood flow in canine jejunal loop in situ. 11 33

Prostaglandin (PG) synthetase activity and selective hormone responsiveness were examined in normal and SV40 transformed WI-38 fibroblasts (VA13-2RA). The transformed VA13-2RA cells have significantly reduced rates of PGE1, PGE2, PGF1alpha and PGF2alpha synthesis as compared to the normal WI-38 fibroblast. The transformed cell in contrast to the normal cell hyperresponds to stimulation by L-epinephrine (10 muM) and PGE1 (8.5 muM) but is unresponsive to bradykinin (BK) as measured by the accumulation of intracellular cyclic AMP. Indomethacin treatment does not significantly alter the PGE1 and L-epinephrine (EPI) responsiveness of the normal WI-38 fibroblast, however it abolishes the BK response in these cells. These results provide further evidence for the dependency of cell activation by bradykinin on the PG synthetase system. No experimental data was found to support the role of PGs as negative regulators of PGE1 and EPI responsiveness in the WI-38 fibroblast. Using the VA13-2RA cells, limited attempts to recover PG synthetase activity comparable to that found in normal WI-38 cells were unsuccessful. The VA13-2RA cell and its normal counterpart represent models for investigating the role of PGs in cell function and the mechanism of BK activation and its effect on cell metabolism.
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PMID:Prostaglandin synthetase activity and hormone responsiveness in normal and SV40 transformed WI-38 fibroblasts. 17 65

Human synovial fibroblasts in culture respond to bradykinin (8 X 10(-9) M) with an increment in intracellular cyclic AMP concentration. These bradykinin (BK) concentrations are comparable to levels of the nonapeptide found in pathological synovial effusions. The cyclic AMP response to BK is enhanced by a heat stable factor(s) in fetal calf serum (FCS) and by the addition of arachidonic acid (AA) to monolayer cultures incubated in serum-free media. Synovial fibroblasts initially treated with BK are refractory to rechallenge with this agent as measured by the absence of an increment in cyclic AMP. These BK refractory cells do respond with significant increment in cyclic AMP to challenge with prostaglandin E1 (PGE1). Cells that have become refractory to PGE1 stimulation respond to BK. this suggests that a receptor or activator system different from the one for PGE1 and PGE2 exists for BK. When both BK and PGE1 are incubated together with synovial fibroblasts, the cyclic AMP response elicited is more than additive as compared to the response of each hormone separately. Indomethacin (IM) inhibits the BK evoked cyclic AMP response unless cell cultures are pretreated with PGE1. The PGE1 analog, 7-oxa-13-prostynoic acid, is a better inhibitor of the cyclic AMP response induced by BK than by PGE1. BK does not elicit a cyclic AMP response solely by elaborating PGE1, yet the prostaglandin pathway and its products seem to have a role in the degree of the cyclic AMP response to BK challenge.
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PMID:Human synovial fibroblasts: the relationships between cyclic AMP, bradykinin, and prostaglandins. 19 39

Isolated rat lung parenchymal strips responded to carbachol, 5-HT and phenylephrine (PE) with contractions. Bradykinin (BK), histamine, PGF2 alpha, PGE1, PGE2 and dimaprit were either inactive or produced weak relaxations. Isoproterenol, noradrenaline (NA) and epinephrine (E) relaxed lung strips. The further increase in their concentrations produced contractions of varying magnitudes. The lung strips contracted to 5-HT or carbachol, responded to isoproterenol and E and NA with relaxations. Metiamide and cimetidine (selective histamine H2-receptor antagonists) did not alter responses to histamine and carbachol. Propranolol (a beta-adrenoceptor blocker) antagnoized or reversed relaxations to E and isoproterenol, and markedly enhanced contractions to NA, PE and E. Atropine and phentolamine or dibenzyline antagonized contractions to carbachol and sympathomimetic agents, respectively. From study it may be concluded that there are alpha- and beta-adrenergic receptors mediating contractions and relaxations in the peripheral airways of rat.
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PMID:Evidence for the existence of alpha-adrenoceptors in the rat lung. 22 16

Production, transport, storage and release of antidiuretic hormone (ADH) in the hypothalamo-neurohypophysial system were investigated. ADH produced by nerve cells in the paraventricular and supraoptic nuclei of the hypothalamus is present in a form bound to the specific protein neurophysin, in the neurosecretary granula. Electric and chemical stimulation of these nuclei results in evoked release of ADH in ionic association with neurophysin from the neural lobes. Acetylcholine, norepinephrine, histamine, angiotensin II, gamma-aminobutyric acid and L-glutamic acid have been regarded as candidates of chemical transmitters for the release of ADH in the hypothalamus. Prostaglandin (PG) E2 may be another important compound for central regulation of water metabolism. The possibility that PGE2 may be the transmitter or a modulator in the nuclei has to be considred. Serotonin, dopamine and taurine, however, may not be involded in the ADH releasing mechanisms in the hypothalamus. It appears that norepinephrine, histamine, angiotensin II, PGE2 and bradykinin stimulate directly the neural lobe to release ADH. The ADH release is regulated by intracellular Ca++. The existence of a "readily-releasable pool" of ADH can be ruled out and any limitation in the amount of ADH released under experimental conditions may be due to insufficient activation of the neural lobe. A physiological significance other than a carrier was proposed for neurophysin.
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PMID:[The hypothalamo-neurohypophysial system and antidiuretic hormone (author's transl)]. 33 45

In order to study the effect of sodium acetylsalicylate and the role of prostaglandins on intradental nerve impulse activity experiments were performed on the teeth of anaesthetized cats. Nerve impulse activity was induced by mechanical and chemical stimuli and recorded by means of electrodes inserted into dentinal cavities. It was shown that such activity could not be blocked by sodium acetylsalicylate or indomethacin given locally or i.v. PGE2 failed to excite the sensory units when given locally (3.5 microng/ml) or intraarterially (35-140 ng/min) alone or in combination with mechanical and thermal stimuli or combined with local application of histamine (10 mg/ml) or bradykinin (10 mg/ml). Intraarterial infusion or arachidonic acid, a precursor to PGE2, PGF2 alpha PGG2 and PGH2 failed to change the excitability even on applying local stimuli to the pulp or with local application of histamine or bradykinin. These findings seem to indicate that the increased sensitivity of the tooth to thermal stimuli seen during acute pulpitis is not due to formation of prostaglandins.
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PMID:Sodium acetylsalicylate and the role of prostaglandins in the mechanism of intradental pain. 40 38


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