UNIPROT:P01042 - FACTA Search

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Query: UNIPROT:P01042 (bradykinin)
15,585 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To extend our recent observations of the possible downregulation of glomerular B2-kinin-binding sites, we investigated density (Bmax) of bradykinin (BK)-binding sites in glomerular membranes of both the clipped (C) and nonclipped (NC) kidneys of two-kidney, one-clip (2K-1C) Goldblatt hypertensive rats, in relation to tissue kallikrein activity and glomerular three-dimensional structure. Compared with the Bmax of sham-operated (SO) kidney (31.8 +/- 7 fmol/mg protein), a significant increase in Bmax was observed in glomeruli of both kidneys in hypertensive rats, the Bmax being higher in glomeruli of NC than in C kidneys (98 +/- 11 vs. 59 +/- 12 fmol/mg protein). NC kidney compensatory hypertrophy was expressed by an increase in glomerular diameter, surface area, and volume. When expressed per unit of area or volume, Bmax in NC kidneys remained significantly higher than in both C and SO kidneys. Increased Bmax in both kidneys of 2K-1C rats was associated with a decreased intrarenal level of kallikrein. We also examined prostaglandin (PG) E2 release by isolated glomeruli from SO, C, and NC kidneys as a possible biological effect induced by BK. Whereas C kidney released more PGE2 than NC kidney under basal conditions, addition of BK (10 nM) induced greater PGE2 production in NC kidney consistent with the difference in Bmax between C and NC kidneys. These results suggest a possible downregulation of glomerular B2-binding sites by bradykinin, which may explain the difference between SO and C kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glomerular B2-kinin-binding sites in two-kidney, one-clip hypertensive rats. 185 18

In many isolated tissues, including glomerular mesangial cells and endothelial cells, the synthesis of platelet activating factor (PAF) occurs by remodeling the phospholipids so that the production of PAF results in the release of arachidonic acid with subsequent production of cyclooxygenase or lipoxygenase products. In some tissues, including the renal medulla, another pathway for PAF biosynthesis (the de novo pathway) has been found in which the production of PAF is not linked to the production of arachidonic acid products. We tested the hypothesis that the remodeling pathway was active in the release of PAF into renal venous effluent of the isolated kidney. Isolated rat kidneys perfused at constant flow with albumin-containing buffer were stimulated to produce prostaglandin by an infusion of angiotensin II or bradykinin. Some kidneys were also challenged with the calcium ionophore A23187. Perfusate was collected for bioassay of PAF and radioimmunoassay of prostaglandin (PG) E2; urine was collected for PAF bioassay. Angiotensin II (10(-9) to 10(-8) M) increased renal vascular resistance, and bradykinin (10(-8) to 10(-7) M) and A23187 (3 x 10(-6) M) reduced renal vascular resistance. PGE2 production was increased significantly by bradykinin and angiotensin II but not by A23187. Only A23187 increased the release of PAF into the perfusate. Urine PAF was not changed by any of the stimuli. These data indicate that the release of PGE2 by the isolated, perfused rat kidney can be dissociated from the release of PAF. The findings support the suggestion that PAF released by the kidney into the renal venous effluent is not produced by remodeling the lipids that are the source of renally released prostaglandins.
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PMID:Release of platelet activating factor by the isolated kidney is not linked to the production of prostaglandins. 194 8

The ability of arachidonic acid (AA) and bradykinin to release calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) from capsaicin-sensitive primary afferents was studied in guinea pig isolated and perfused heart. Infusion of AA (50 microM to 5 mM, 0.5 ml/min over 2 min) produced a remarkable and dose-dependent CGRP-LI release that was abolished by in vitro capsaicin (10 microM) pretreatment or in the presence of indomethacin (10 microM). The capsaicin antagonist ruthenium red (10 microM) did not affect the CGRP-LI release produced by AA, whereas it blocked that produced by capsaicin (10 microM). In vitro capsaicin pretreatment reduced the increase in heart rate evoked by AA, whereas it did not affect the increase in coronary flow and decrease in contractility. Bradykinin (10 microM, 0.5 ml/min over 2 min) induced CGRP-LI release in a similar manner to that produced by AA, with the only difference being that in the presence of indomethacin, a residual increase in CGRP-LI outflow was still observed. AA increased the outflow of 6-keto-prostaglandin (PG) F1 alpha, PGE2 and leukotriene B4, whereas bradykinin enhanced only the release of 6-keto-PGF1 alpha. Infusion of either PGI2 or PGE2 (1-100 microM) released CGRP-LI in a dose-dependent manner and with a similar potency. PGI2 (100 microM)- or PGE2 (100 microM, 0.5 ml/min over 2 min)-evoked release was abolished by previous exposure to capsaicin and not affected by indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arachidonic acid and bradykinin share a common pathway to release neuropeptide from capsaicin-sensitive sensory nerve fibers of the guinea pig heart. 194 23

The experiments described in this article were designed to investigate the regulation of, and functional response to, prostaglandin (PG) synthesis in cultured bovine glomerular endothelial cells. Glomerular endothelial cells in culture synthesized PGE2 much greater than PGF2 alpha greater than thromboxane A2 greater than PGI2 in the presence of 30 microM arachidonate. Basal levels of PGE2 synthesis in these cells were one sixth less than that of bovine mesangial cells. PGE2 synthesis was time dependent and required the continuous presence of serum. Moreover, PGE2 synthesis was regulated by phospholipase A2 as shown by ionomycin-stimulated PGE2 accumulation as well as by bradykinin- and thrombin-stimulated PGE2 accumulation. Even though acidic fibroblast growth factor and heparin were required to support glomerular endothelial cell growth in culture, these agents downregulated PGE2 synthesis. PG endoperoxide synthase activity, as shown by arachidonate-stimulated PGE2 accumulation, also regulated PGE2 synthesis. PGE2 and PGF2 alpha, as well as thromboxane A2 and PGI2 mimetics (1 microM) evoked mitogenesis in quiescent glomerular endothelial cells. PGE2 and PGF2 alpha were most potent, and threshold doses of these PG were 10 nM. These data suggest that glomerular endothelial cells are similar to other microvascular endothelial cells in their regulation of PG synthesis and that, under physiological conditions, the proliferation of glomerular endothelial cells might be regulated by PG in an autocrine or paracrine fashion.
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PMID:The regulation and role of prostaglandin biosynthesis in cultured bovine glomerular endothelial cells. 195 28

Effects of exogenous prostaglandin (PG) E2 and PGI2 on testicular polymodal receptor activities were compared in in vitro recordings of single- or multi-fiber discharges from canine testis-spermatic nerve preparations. PGI2 up to 1.4 x 10(-6) mol/l (cumulative method) or 1.0 x 10(-5) mol/l (non-cumulative method) excited only weakly some of the receptors, and similar observations were made with PGE2. Both PGs applied cumulatively or non-cumulatively at concentrations above 1.4 x 10(-8) mol/l augmented the response to bradykinin (9.4 x 10(-8) mol/l) in more than half of the cases tested. The augmenting effect of PGE2 lasted longer than that of PGI2 both with the cumulative and the non-cumulative method. The degree of augmentation tended to increase dependent on concentration, but some cases showed no further increase or rather a decrease in augmentation by PGs at a ten times higher concentration, especially when PGs were applied cumulatively. A second challenge by PG after a short interval (2 min) did not induce augmentation. These phenomena were considered to be tachyphylaxis to PGs. Cross-tachyphylaxis to PGE2 and PGI2 was also observed. There was not much difference in excitatory and augmenting potencies between these two PGs, but there was a clear difference in the concentrations of the PGs necessary to induce excitation of polymodal receptors and to facilitate their response to bradykinin.
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PMID:Comparison of the effects of prostaglandins E2 and I2 on testicular nociceptor activities studied in vitro. 196 Dec 61

We assessed the role of bradykinin (BK) in allergen-induced early and late bronchial responses, airway inflammation, mediator release, and antigen-induced airway hyperresponsiveness in allergic sheep by studying the effects of the BK B2 receptor antagonist, NPC-567 (D-Arg-[Hyp3, D-Phe7]-BK), on these parameters. Antigen challenge was performed on two occasions greater than 3 wk apart, once with placebo (control) and once after high-dose (10 mg/ml) and low-dose (5 mg/ml) treatments with aerosol NPC-567. In the control trials (n = 14) antigen challenge resulted in an early and late increase in specific lung resistance (SRL). The early response was associated with increases (p less than 0.05) in prostaglandin (PG) D2, immunoreactive kinin, tosyl-L-arginine methyl ester (TAME)-esterase, and PGE2 in bronchoalveolar lavage (BAL) fluid. The late response was associated with increases (p less than 0.05) in leukotrienes (LT) B4 and C4, thromboxane (TX) B2, 6-keto-PGF10, and PGE2. There was a significant influx of neutrophils in the BAL fluid during the late response, and airway hyperresponsiveness to carbachol aerosol was apparent 4 h after challenge. In six sheep the high-dose NPC-567 treatment (given before, during, and 4 h after antigen challenge) did not attenuate the early bronchoconstrictor response or the early release of mediators but caused a significant reduction in the late response (p less than 0.05). This protective effect was accompanied by reductions (p less than 0.05) in both the concentrations of all the mediators associated with the late response and the severity of the BAL neutrophilia. High-dose NPC-567 did not attenuate the airway hyperresponsiveness or the cellular inflammatory response seen 24 h after challenge. In eight sheep treated with the low dose of NPC-567 (given before, during, and 4, 8, and 24 h after challenge) the early response was not blocked but the late response was again inhibited, as were the mediators associated with the late response. At the low dose the drug did not prevent the airway inflammation at 8 or 24 h. The additional treatments did, however, prevent the 24 h hyperresponsiveness. These data suggest that kinin generation during antigen-induced airway anaphylaxis may be important for controlling the release of arachidonic acid metabolites from airway inflammatory cells that contribute to the development of the late response in the allergic sheep model.
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PMID:A bradykinin antagonist modifies allergen-induced mediator release and late bronchial responses in sheep. 200 91

Neurohistochemical and in vivo and electron microscopic methods demonstrated alpha-and beta-adrenergic receptors and adrenergic innervation in arterioles and "arterial" capillaries of the mouse spleen. Such innervation and receptors in venules and channels within the red pulp were sparse. Cholinergic innervation and receptors were judged to be absent in the microvasculature. Histamine elicited arteriolar dilation which was blocked by metiamide suggesting the presence of H2 receptors. However, following blockade of H2 receptors, histamine produced arteriolar constriction. Serotonin elicited only venular constriction. Lactic acid caused arteriolar constriction; bradykinin and prostaglandins (PG) E2 and PGF2 alpha triggered arteriolar constriction, but only at higher concentrations. The vasoconstriction evoked by cholinergic agonists, histamine, lactic acid, or PGs was partially or completely antagonized by alpha-adrenoceptor blockade or by reserpine, and the vasoconstrictor responses to histamine, lactic acid, PGs, bradykinin were enhanced in the presence of functional adrenergic nerves. In the latter case higher doses of phentolamine provoked arteriolar vasospasm. Although adenine nucleotides, guanosine, inosine, sodium phosphate, and sodium chloride elicited no response, adenosine was a potent vasodilator. This dilation was not blocked by beta-adrenergic antagonists, and it was enhanced in the presence of functional adrenergic nerves. The data suggest that: (1) cholinergic agonists, lactic acid, histamine, and PGE2 and PGF2 alpha cause alpha-mediated arteriolar constriction by releasing stored neurotransmitter(s) from splenic nerves, and (2) subthreshold quantities of neurotransmitter(s) may modulate microvascular sensitivity to vasoactive agents which act directly upon the vascular wall.
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PMID:Innervation and vascular pharmacodynamics of the mouse spleen. 205 23

To investigate whether altered renal medullary prostaglandin (PG) synthesis is involved in the development of hypertension in spontaneously hypertensive rats (SHR), we compared the hormonal responsiveness of cultured renal papillary collecting tubule (RPCT) cells from SHR and Wistar-Kyoto rats (WKY) as control. Basal levels of PGE2 and cAMP were lower in 4-weeks-old SHR than in WKY, while PGE2 synthesis after stimulation with arachidonate, A23187 or bradykinin and the level of cAMP responded to vasopressin or exogenous PGE2 were similar in both strains. There was no difference in basal nor stimulated levels of cGMP between both strains. In 16-week-old rats, basal levels of cAMP, cGMP and PGE2 were significantly lower than in 4-week-old rats, but no differences were recognized between both strains. These results suggest that RPCT cells of SHR and WKY at the post-weaning period may differ in the metabolism of PGE2 and cAMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.
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PMID:[Responsiveness of cultured papillary collecting tubules to vasoactive hormones: comparison between spontaneously hypertensive rats and Wistar-Kyoto rats]. 206 16

The role of PGE2 in the sensitization of high-threshold tarsal joint mechanoreceptors (putative nociceptors) has been investigated in 11 arthritic and 16 normal rats. Injections of a low dose of Freund's complete adjuvant at multiple sites into the tissues surrounding the ankle joint induced a chronic unilateral monoarthritis in the injected limb. Measurements of both spontaneous activity and responses of tarsal joint mechanoreceptors to repeated graded mechanical stimuli were made. All of the mechanoreceptors examined had afferent fibres with conduction velocities in the C- or A-delta range. Using this new model of joint inflammation we have shown that lysine acetylsalicylate reduces the mechanical sensitivity of these joint mechanoreceptors and reduces the spontaneous activity in afferent nerve fibres. Prostaglandin E2 is unable to restore either the spontaneous activity in the afferent axon or the mechanical sensitivity of tarsal joint mechanoreceptors after lysine acetylsalicylate in the arthritic rat. Similarly, PGE2 does not sensitize or excite tarsal joint mechanoreceptors in the normal rat. In the normal rat, however, PGE2 potentiates the excitatory action of bradykinin and enhances the sensitizing effect of bradykinin on the responses of joint mechanoreceptors to mechanical stimulation when both substances are injected simultaneously. These results indicate that PGE2 is not important in the sensitization of these joint mechanoreceptors in this model of chronic joint inflammation but that in other circumstances PGE2 may be able to contribute to a sensitization of joint mechanoreceptors by enhancing the action of bradykinin.
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PMID:The role of PGE2 in the sensitization of mechanoreceptors in normal and inflamed ankle joints of the rat. 206 45

The relative potencies of PGD2, PGE2 and PGI2 in potentiating bradykinin-induced hyperalgesia and oedema were determined in the paws of aspirin-treated guinea-pigs. PGE2 and to a lesser degree PGD2 but not PGI2, potentiated bradykinin-induced hyperalgesia, whereas PGD2, but not PGE2 or PGI2, potentiated oedema. These findings differ from those in other species, and possibly reflect interspecies differences in modulation of inflammatory reactions by prostanoids.
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PMID:Prostaglandin (PG) modulation of bradykinin-induced hyperalgesia and oedema in the guinea-pig paw--effects of PGD2, PGE2 and PGI2. 206 78

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