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)

To study the effects of stimulation of renal prostaglandin biosynthesis by bradykinin, we assessed the changes in renal functions induced by intrarenal infusion of bradykinin (10 ng . min-1 . kg-1) in the dog anesthetized with pentobarbital before and during inhibition of prostaglandin synthesis by sodium meclofenamate (5 mg/kg). Before meclofenamate administration, bradykinin augmented the urinary output of a "PGE"-like substance from 1.00 +/- 0.25 to 3.88 +/- 1.09 ng/min (P less than 0.05) and increased renal blood flow by 65 +/- 9 ml/min (P less than 0.001), urine flow by 0.55 +/- 0.23 ml/min (P less than 0.05), and sodium excretion by 64.8 +/- 18.0 mueq/min (P less than 0.01). Administration of meclofenamate did not affect the bradykinin-induced increase in renal blood flow and urine volume, but suppressed the evoked output of "PGE" and reduced the associated natriuresis, i.e., sodium excretion increased by only 11.1 +/- 4.8 mueq/min (P greater than 0.05). In contrast, meclofenamate did not affect the natriuresis effected by an equidilator dose of PGE2 (5 ng . min-1 . kg-1) infused intrarenally. These observations suggest that a product of prostaglandin synthetase produced by the kidney during intrarenal infusion of bradykinin contributes to the natriuretic action of the peptide.
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PMID:Contribution of renal prostaglandins to the natriuretic action of bradykinin in the dog. 47 58

1 In the isolated kidney of the rabbit perfused with oxygenated Tyrode solution, we studied the effect of bradykinin on the vasoconstriction evoked by sympathetic nerve stimulation (3Hz, 1 ms) and by injections of noradrenaline (50 to 75 ng) in the presence and in the absence of indomethacin (1 microgram/ml), an inhibitor of prostaglandin biosynthesis. Prostaglandin E(PGE)-like material in the renal effluent was measured by bioassay after extraction with organic solvents and separation by thin layer chromatography. 2 Bradykinin in concentrations of 10 to 100 ng/ml reduced the vasoconstrictor response to sympathetic nerve stimulation and to injected noradrenaline. Also, the peptide (1 to 10 ng/ml) increased the basal release of PGE-like material and the release induced by sympathetic nerve stimulation. 3 Indomethacin, 1 microgram/ml, diminished the inhibitory effect of bradykinin on the vasoconstrictor response to nerve stimulation, minimized the reduction of the noradrenaline-induced vasoconstriction caused by bradykinin (100 ng/ml), and abolished the release of PGE-like material. 4 This study indicates that bradykinin reduces the renal vascular reactivity to adrenergic stimuli and suggests that part of the action of the kinin at the vascular adrenergic neuroeffector junction in the rabbit kidney depends upon the biosynthesis of renal prostaglandins.
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PMID:Attenuation by bradykinin of adrenergically-induced vasoconstriction in the isolated perfused kidney of the rabbit: relationship to prostaglandin synthesis. 49 30

The i.v. administration of 0.25 mg/kg SQ 20881 to eight renal hypertensive patients caused blood pressure fall and in five of them also reduced heart rate. The latter was attributed to increase in vagal tone. Peripheral and renal blood samples taken at the nadir of the hypotensive response showed considerable inhibition of plasma kininase activity, rise in free kinin level and reduced kininogen content. This reduction was not due to increased consumption as shown by in vitro experiments. PGE2 and PGF2 alpha levels in kidney blood of three patients remained practically unchanged. Plasma renin activity was augmented to a larger extent in blood of kidney with stenotic artery than in the one with patent vessel. It is concluded that the action of SQ 20881 on human blood kinin system, besides inhibition of kininase, involves also reduction of kininogen, the mechanism of which remains to be clarified.
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PMID:Blood kinin system in renal hypertensive patients administered with SQ 20881. 51 51

Ethanolamine plasmalogens (1-alk-1'-enyl-2-acyl-sn-glycero-3-phosphoethanolamines) of many tissues contain high levels of arachidonate at their 2-position, and in certain tissues have been implicated as possible donors of arachidonate required in the synthesis of prostaglandins and thromboxanes. In the present study, [3H]arachidonate-labeled phospholipids of HSDM1C1 cells, a cell line derived from a mouse fibrosarcoma, were examined to determine the donor of the arachidonic acid released upon bradykinin stimulation of the synthesis of PGE2. HSDM1C1 cells labeled with [3H]arachidonic acid for 24 hr in serum-free medium were used in most of the experiments and had the following distribution of label among the cellular lipids; phosphatidylcholine (33%), phosphatidylinositol (20%), diacyl-sn-glycero-3-phosphoethanolamine (15%), ethanolamine plasmalogen (15%), and less polar lipids )16%). Bradykinin treatment stimulated a rapid hydrolysis of [3H]arachidonate from the cellular lipids and conversion of the released acid to PGE2, which was secreted into the medium. The label was released predominantly from phosphatidylinositol and possibly from phosphatidylcholine with no detectable change in the labeling of diacyl- or 1-alk-1'-enyl-2-acyl-sn-glycero-3-phosphoethanolamine. The ethanolamine plasmalogens, therefore, do not appear to be involved in the stimulated release of arachidonate in the HSDM1C1 cells. Indomethacin blocked the bradykinin-stimulated synthesis of PGE2 and to a lesser degree inhibited the release of [3H]arachidonate from the cellular lipids into the medium.
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PMID:Bradykinin-stimulated release of [3H]arachidonic acid from phospholipids of HSDM1C1 cells: comparison of diacyl phospholipids and plasmalogens as sources of prostaglandin precursors. 53 Dec 22

1. Renal arterial infusions of endogenous vasoactive compounds were administered, and elctromagnetic flow probes were used to measure simultaneous ipsilateral and contralateral renal blood flow. 2. The expected ipsilateral renal blood flow changes resulting from infusions of acetylcholine, noradrenaline, angiotension II, bradykinin and PGE2 were observed. There were no transient, phasic or sustained contralateral renal blood flow changes. 3. These results suggest that a previously hypothesized reno-renal vasomotor reflex communication does not exist. The discrepancies between these present studies and previous ones proposing such a reflex may be due to the methods chosen for measurement of renal blood flow.
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PMID:Evaluation of drug-induced reno-renal vasomotor reflex in the dog. 58 74

The effects of prostaglandin E1 (PGE1), PGE2, PGF2a, PGA1, bradykinin, and adenosine on uterine blood flow and intrauterine pressure were compared with that of estradiol-17beta in ovariectomized, estradiol-treated ewes. PGE1 and adenosine increased uterine blood flow, measured with implanted electromagnetic flow probes encircling each uterine artery, to levels comparable to those induced by estradiol, which averaged 116 ml/minute. PGE2, PGA1, and bradykinin increased blood flow 20, 36, and 80% of that caused by estradiol. Adenosine produced a flow comparable to the maximal estradiol response. PGE2 and PGF2a decreased peak estradiol-induced uterine flow 50 and 70%, yet increased uterine pressure. The effects of PGE2 appeared to be mediated by myometrial activity; PGE1 could possibly mediate estrogen-induced uterine vasodilation.
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PMID:The effect of prostaglandins and other vasoactive substances on uterine blood flow and myometrial activity. 61 33

A defective prostaglandin metabolism in patients with erythromelalgia may explain several of the clinical features of this condition, such as the red discoloration and burning sensations of the skin. In two patients with erythromelalgia a grossly abnormal bullous reaction to intradermally injected PGE1, PGE2, and PGF1alpha occurred, whereas a normal reaction appeared after injection of histamine, serotonin, and bradykinin. Furthermore, prostaglandin-like material was detected in increased concentration in skin perfusates from these patient. In PGE1-equivalents the concentration amounted to 2.0 and 3.2 ng/ml of the original perfusate, as compared to 0.1 ng/ml in normal skin. The capacity of synthesizing prostaglandins was increased in skin biopsy material from both patients. At least part of the therapeutic effect of aspirin in these patients may be due to the influence of this drug on prostaglandin metabolism.
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PMID:Pathogenesis of erythromelalgia. 61 69

1 The responses of circularly cut strips of cervix and uterine horn from rats on days 20 and 22 of pregnancy to drugs were compared in vitro. 2 The cervix exhibited similar responses and sensitivities to acetylcholine, bradykinin, prostaglandin (PG) F2alpha (day 20) and isoprenaline (day 20) as did the uterine horn but was less sensitive or responded less consistently to isoprenaline (day 22), oxytocin and PG1. PGE2 was more potent on the cervix (day 20). 3 Before term the relatively inextensible connective tissue of the cervix plus contractions of the smooth muscle would help to prevent foetal expulsion. At term the cervical smooth muscle is sufficiently unresponsive to allow cervical dilatation.
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PMID:Mechanical responses of the isolated cervix and uterine horn of pregnant rats near term to drugs. 66 96

The hamster cheek pouch prepared for intravital observations on macromolecular permeability with fluorescein labelled dextran was used in four series of 5 hamsters each, all pretreated with indomethacin. Bradykinin, PGE1, PGE2 and PGF2alpha increased macromolecular leakage at postcapillary venules, and this leakage was reversible on removal of agent. A linear relation was found between the logarithmic value of dose of bradykinin and the mean number of leakage sites. No tachyphylaxis to bradykinin was seen. The effect of either PGE1, PGE2 or PGF2alpha applied simultaneously with bradykinin was to significantly (p less than 0.05) potentiate the bradykinin response. Bradykinin and these prostaglandins appeared to have the same site of action for their effect of increasing permeability, e.g. the postcapillary venule.
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PMID:Bradykinin and prostaglandin E1, E2 and F2alpha-induced macromolecular leakage in the hamster cheek pouch. 72 17

The preparation and use of the rabbit transverse stomachstrip as an isolated assay tissue for prostaglandins is described. The tissue is relaxed by low concentrations of PGE2, PGA2 and PGD2 and contracted by prostacyclin (PGI2) and PGF2alpha. The decomposition product of prostacyclin, 6-oxo-PGF1alpha, has little effect, whereas the endoperoxide PGH2 and thromboxane A2 cause a small contraction. Arachidonic acid also contracts the tissue and this response is abolished by indomethacin. This tissue also responds to low concentrations of histamine, acetylcholine, noradrenaline and bradykinin. In conjunction with other bioassay tissues such as the rat stomach strip and rabbit coeliac artery, the rabbit transverse stomach strip provides a convenient method of detection of identification of known arachidonic acid metabolites.
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PMID:Use of the rabbit transverse stomach-strip to identify and assay prostacyclin, PGA2, PGD2 and other prostaglandins. 75 96


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