Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0432222 (SEM)
47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anaphylactoid reactions (AR) are the most feared complications of hemodialysis. Recently, a high incidence of AR has been reported during dialysis with AN69 membranes in patients treated with ACE inhibitors. Plasma levels of C3a, histamine and bradykinin were measured in 12 patients at the onset of AR during dialysis with AN69. We also investigated bradykinin generation in 10 symptom-free patients dialyzed with four different membranes. None of the 12 patients studied during AR displayed excessive complement activation or histamine release. In contrast, high bradykinin plasma levels (2392 +/- 53 fmol/ml; mean +/- SEM) were observed in all nine patients of whom bradykinin was measured. One patient developed two consecutive episodes of hypersensitivity on AN69 membranes even without taking ACE inhibitors. Bradykinin levels were high in both episodes (5280 and 10467.7 fmol/ml). Furthermore, this patient showed no symptoms and normal bradykinin levels (123.4 fmol/ml) when dialyzed with other membranes. The role of the membrane type in the AR is further substantiated by the observation that AN69 also provoked a significantly higher bradykinin generation (327.6 +/- 18 fmol/ml; mean +/- SEM) during symptom-free sessions compared to other membranes like CuprophanR (5.1 +/- 7.3), HemophanR (17.2 +/- 6.3) and PolysulfoneR (39.7 +/- 6.6). Our findings strongly suggest that bradykinin is the principal mediator of AR during hemodialysis with AN69 membranes. To our knowledge it is the first time that data support the hypothesis of a more general role of bradykinin in shock-like symptoms. Furthermore, bradykinin generation must be regarded as a new marker of biocompatibility of extracorporeal treatments.
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PMID:Bradykinin is a mediator of anaphylactoid reactions during hemodialysis with AN69 membranes. 807 63

It has been shown that suboptimal preparation of a vein graft prior to its insertion results in immediate morphologic and functional damage to the endothelial cells but not to the underlying smooth muscle cells. However, little is known about whether such perioperative injury to the vein grafts influences the subsequent development of intimal hyperplasia and smooth muscle cell contractility. This study examines the influence of storage in saline solution or Ringer's lactate on the development of intimal hyperplasia and vasomotor function in experimental vein grafts. Twenty-six New Zealand white rabbits had a carotid vein bypass graft performed after the veins had been immersed (15 minutes) in either heparinized saline solution (Sal; n = 13) or Ringer's lactate (RL; n = 13), and each group was harvested after 28 days for either histologic (n = 8) or functional studies (n = 5; four 5 mm rings/graft). Saline storage of the vein graft resulted in a 38% increase in the thickness of the intimal hyperplasia (113 +/- 2 vs. 83 +/- 2 microns, Sal vs. RL; mean +/- SEM; p < 0.05) without a change in medial thickness (87 +/- 5 vs. 86 +/- 8 microns, Sal vs. RL; p > 0.05). The two sets of vein grafts showed no difference in sensitivity to norepinephrine, serotonin, and bradykinin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of perioperative storage solutions on long-term vein graft function and morphology. 819 48

Bradykinin (BK) and its analogs (1 nM-100 microM) stimulated phosphoinositide (PI) turnover in murine fibrosarcoma (HSDM1C1) cells in a concentration-dependent manner. The relative potencies (EC50) were: BK = 48 +/- 4 nM; Lys-BK = 39 +/- 3 nM; Met-Lys-BK = 158 +/- 33 nM, Des-Arg9-BK = 2617 +/- 598 nM (means +/- SEM, n = 3-14). All these analogs were full agonists and they produced up to 5.4 +/- 0.4-fold stimulation of PI turnover at the highest concentration (10-100 microM) of the peptides. In contrast, the analogs [D-Arg0-HYP3-Thienyl5,8-D-Phe7]-BK (HYP3-antagonist), [D-Arg0-HYP3-Thienyl,5,8-D-Phe7]-BK (Thienyl antagonist) and Des-Arg9-Leu8-BK were inactive, as agonists, at 0.1 nM-1 microM in this system. These data suggested that BK-induced PI turnover in these cells was mediated via B2-type of BK receptors. This was confirmed further by the fact that both the B2-selective Hyp3- and Thienyl-antagonists inhibited BK-induced PI turnover with KBS of 369 +/- 51 nM and 368 +/- 118 nM respectively while the B1-selective antagonist, Des-Arg9-Leu8-BK, was inactive at 1 microM. [3H]BK receptor binding studies revealed two binding sites, one with high affinity (Kd = 0.24 +/- 0.06 nM; Bmax = 1.4 +/- 0.4 pmol/g tissue) and the other with low affinity (Kd = 18.5 +/- 0.95 nM; Bmax = 25.1 +/- 0.52 pmol/g tissue), on HSDM1C1 cell homogenates. The rank order of affinity of BK analogs at inhibiting specific [3H]BK binding was similar to that found for PI turnover.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The neuropeptide bradykinin stimulates phosphoinositide turnover in HSDM1C1 cells: B2-antagonist-sensitive responses and receptor binding studies. 827 96

Tannin, isolated from aqueous extracts of cotton bracts, inhibits chloride secretion in airway epithelial cells. The effect of tannin on the epinephrine- and bradykinin-stimulated rise in intracellular free calcium and cyclic adenosine monophosphate (cAMP) was examined using bovine tracheal epithelial cells in suspension and culture. Basal intracellular calcium levels were 33 +/- 11 nM (mean +/- SEM, n = 54) and increased 13- to 15-fold after addition of epinephrine (10(-6) M) or bradykinin (2 x 10(-6) M). Tannin pretreatment blunted the subsequent response to epinephrine beginning at a tannin concentration of 10 micrograms/ml. Pretreatment with 100 micrograms/ml tannin completely inhibited the rise in intracellular free calcium in response to epinephrine but had no effect on the calcium response to bradykinin. In the absence of tannin, both bradykinin and epinephrine increased intracellular levels of cAMP. At a tannin concentration of 10 micrograms/ml, tannin inhibited the rise in intracellular cAMP in cells stimulated with either epinephrine or bradykinin but had no effect on bradykinin-stimulated prostaglandin E2 release. Tannin alone (10 micrograms/ml) increased prostaglandin E2 release. In other studies, tannin inhibited epinephrine binding to airway epithelial cells in a dose-dependent manner. R(o) decreased from 948 +/- 69 fmol/mg protein under control conditions (n = 4) to 587 +/- 131 fmol/mg protein in the presence of 25 micrograms/ml tannin (n = 3). Tannin had no effect upon the Kd for epinephrine binding (132 +/- 12 pM). Tannin had no effect on bradykinin binding to airway epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tannin inhibits cAMP pathways in bovine airway epithelium. 829 75

Capillary barrier function is subject to changes in Starling forces via hemodynamic status (hydrostatic pressure) or protein milieu of fluids bathing the wall (oncotic pressure). Venular function is sensitive to inflammatory mediators leading to white cell sticking, fluid and formed element extravasation, and flow disruption. Thus, we hypothesized that vasoactive hormones and autocrines alter preferentially the venular-capillary (VC) barrier. Hydraulic conductivity (Lp) of frog mesenteric venular- and true-capillaries (TC) was measured by the modified-Landis technique under control (LpC), then during atrial natriuretic peptide (ANP, 10(-7) to 10(-8) M), bradykinin (BKN, 10(-7) M), acetylcholine (ACh, 10(-6) to 10(-5) M), angiotensin II (AII, 10(-7) M), or norepinephrine (NE, 10(-6) M) perfusion. All agents, except AII or NE, elevated Lp: LpANP/LpC = 2.9 +/- 0.3 (mean +/- SEM; (n = 55), LpBKN/LpC = 3.3 +/- 0.8 (n = 16), LpACh/LpC = 1.6 +/- 0.1 (n = 26), LpAII/LpC = 1.1 +/- 0.2 (n = 8), and LpNE/LpC = 1.1 +/- 0.2 (n = 9). Contrary to our hypothesis, VC and TC responded similarly: 3.0 versus 2.9 for ANP, 3.4 versus 3.2 for BKN, and 1.6 versus 1.6 for ACh, respectively. These data are consistent with putative vasodilators lowering capillary barrier resistance independent from changes in Starling forces.
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PMID:Vasoactive hormones and autocrine activation of capillary exchange barrier function. 831 66

We examined the actions of potentially natriuretic autacoids in the isolated perfused cortical collecting duct (CCD) dissected from inbred Dahl (Rapp strain) salt-sensitive rats (SS). Atrial natriuretic peptide (ANP, 10 nM), bradykinin (BK, 10 nM), and clonidine (1 microM) were studied to determine their effects on the lumen-to-bath flux of 22Na+ (J1-->b, pmol min-1 mm-1), hydraulic conductivity (Pf, micron/s), and transepithelial voltage (VT, mV). ANP and BK have been shown by others to significantly reduce net Na+ reabsorption and hydraulic conductivity in the Sprague-Dawley (SD) rat CCD, but previous results from our laboratory showed no ANP or BK effect in the SD CCD. In the present study, we were also unable to observe any effect of either ANP or BK in the SS rat CCD. However, in the presence of AVP, clonidine (a partial alpha 2-adrenergic receptor agonist) significantly reduced J1-->b and Pf from 139 +/- 6 (SEM) to 88 +/- 7 and from 959 +/- 176 to 490 +/- 73, respectively. In addition, clonidine significantly depolarized VT from -14.5 +/- 2.8 to -11.2 +/- 1.8. However, unlike its effects in the SD rat CCD, yohimbine (300 nM, an alpha 2-adrenergic receptor antagonist) did not significantly reverse the effects of clonidine on J1-->b, Pf or VT in the SS rat CCD.
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PMID:Clonidine, but not bradykinin or ANP, inhibits Na+ and water transport in Dahl SS rat CCD. 835 63

There are several reports indicating that parathyroid hormone (PTH), besides inducing the formation of cyclic adenosine monophosphate (cAMP), also causes an increase in cytoplasmic free Ca2+ ([Ca2+]i) in osteoblasts, and it has been speculated that both of these second messengers are necessary to mediate PTH-induced bone resorption. In the osteoblastic cell line MC3T3-E1, bovine PTH 1-34 (10 nmol/l-1 mumol/l) stimulated cAMP formation but did not cause an increase in [Ca2+]i in adherent single cells (basal [Ca2+]i = 151 +/- 5 nmol/l, mean +/- SEM; N = 98). In contrast, subsequent addition of bradykinin (1 mumol/l) resulted in a transient increase in [Ca2+]i from a basal level of 155 +/- 11 nmol/l to a peak value of 351 +/- 60 nmol/l (N = 14). When the PTH challenge was followed by the addition of thrombin (10 U/ml), the latter induced a transient rise in [Ca2+]i from a basal level of 173 +/- 12 nmol/l to a peak at 341 +/- 33 nmol/l (N = 20). Primary cultures of human osteoblasts were obtained from trabecular bone. These cells were also PTH-responsive in terms of cAMP formation. On the other hand, human PTH 1-34 (100 nmol/l) did not affect [Ca2+]i in the isolated human osteoblasts, while bradykinin (1 mumol/l) caused a transient increase in [Ca2+]i (from a basal value of [Ca2+]i at 154 +/- 10 nmol/l to a peak value of 757 +/- 147 nmol/l within 30 s; N = 16).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid hormone is able to enhance cyclic adenosine monophosphate formation without causing an increase in cytoplasmic Ca2+ in osteoblasts. 839 31

The dorsal hand vein compliance technique was used to study direct vascular effects of human neuropeptide Y in vivo. Human neuropeptide Y is an endogenous vasoconstrictor peptide that is costored with norepinephrine in sympathetic nerve endings and coreleased with the catecholamine under various physiologic and pathologic conditions. Compared with the alpha 1-adrenergic agonist phenylephrine (geometric mean dose-rate that produces the half-maximal response [ED50]: 1.05 nmol/min; maximum venoconstriction [Emax] +/- SEM, expressed as a percentage of baseline compliance: 91% +/- 3%), human neuropeptide Y was nine times more potent (geometric mean ED50: 0.122 nmol/min; p < 0.001) but markedly less efficacious (Emax: 58% +/- 4%; n = 12; p < 0.001). Venoconstrictor effects of human neuropeptide Y lasted several hours and were unchanged by simultaneous administration of alpha-adrenergic antagonists but were readily reversed by nitroglycerin or bradykinin. The high responsiveness of subcutaneous veins to human neuropeptide Y indicates that human neuropeptide Y may regulate venous compliance and filling of the venous subcutaneous capacitance bed in vivo.
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PMID:Neuropeptide Y in human hand veins: pharmacologic characterization and interaction with cyclic guanosine monophosphate-dependent venodilators in vivo. 852 33

Biochemical signaling determines the specific action of vasomediators in the control of microvascular permeability and tone. We tested the hypothesis that nitric oxide (NO) synthesis is involved in the biochemical signaling pathway of platelet activating factor (PAF). The cheek pouch of anesthetized male Syrian hamsters was used as a microvascular model. Vessel diameter [expressed as the ratio of the experimental to the control (e/c) diameter, with control diameter normalized to 1] and extravasation of FITC-dextran 150 by integrated optical intensity (IOI) were determined using intravital fluorescent microscopy and computer-assisted digital image analysis. N-Nitro-L-arginine methyl ester (L-NAME) at 10(-5) and 10(-6) M and N-nitro-L-mono-methyl arginine (L-NMMA) at 10(-4) and 10(-5) M were used as inhibitors of NO synthase (NOS). Acetylcholine (ACh) and bradykinin were used as indirect indices of NOS activation. L-NAME and L-NMMA attenuated both ACh and bradykinin vasodilatory effects as well as the bradykinin-induced increase in vascular permeability. Topical PAF (10(-7) M) caused vasoconstriction (mean +/- SEM e/c ratio = 0.3 +/- 0.1) and increased IOI from a normalized baseline of 0 to 67.4 +/- 12.8. Topical administration of L-NAME produced differential effects on the series-arranged arterioles but had no effect on postcapillary venular permeability. L-NMMA did not influence the basal arteriolar diameter, but at 10(-5) M it caused a small increase in permeability (IOI = 14.3 +/- 4.2). In the presence of NOS inhibitors, PAF caused a reduced arteriolar constriction (e/c ratio = 0.6 +/- 0.1) relative to PAF alone. Both NOS inhibitors reduced the PAF-stimulated increase in vasopermeability. At 10(-5) M L-NMMA, the PAF-stimulated IOI mean value was 26.1 +/- 5.2, while at 10(-4) M L-NMMA the PAF-stimulated IOI was 15.2 +/- 2.6 compared to 10(-7) M PAF (67.4 +/- 12.8). These results support our hypothesis that NO synthesis is a step in the biochemical signaling pathway of the postcapillary cellular responses to PAF.
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PMID:Platelet activating factor modulates microvascular permeability through nitric oxide synthesis. 853 2

The effect of different dialysis modes on kinin kinetics was studied in seven stable haemodialysis patients treated with AN69 dialysers and ACE inhibitors (ACEI). AN69 haemodiafiltration with calcium-enriched substitution (HDF), AN69 haemodialysis with 1.75 (HD 1.75) and 1.50 (HD 1.50) mmol/l dialysate calcium, AN69 haemodialysis with 1.25 mmol/l dialysate calcium and substitution of 2.25 mmol/h calcium (HD+Ca), and cellulose acetate haemodiafiltration (CA HDF) were compared. Dialysis was uneventful in all patients. During dialysis, serum calcium, sodium, pH, albumin, and bradykinin were measured at the start and after 5 min at arterial, venous, and postinfusion side of the extracorporeal circuit. Serum predialysis bradykinin was 107 +/- 18fmol/ml (mean +/- SEM) in patients on HDF, 61 +/- 9 fmol/ml in patients on HD 1.50, 49 +/- 13 fmol/ml in patients on HD 1.75, 35 +/- 3 fmol/l in patients on HD+Ca, and 75 +/- 27 fmol/ml in CA HDF. No significant change of mean bradykinin levels occurred after 5 min at the arterial and venous side of the dialyser or postinfusion. Individual high bradykinin levels, up to 2672 fmol/ml, were observed but without clinical consequences, suggesting that the threshold value is difficult to determine. No significant correlations were evidenced between bradykinin levels and any of the biochemical measurements. The present data show an intraindividual variability of the bradykinin levels with variation coefficients ranging from 0.386 to 2.783. The present study illustrates that haemodialysis and haemodiafiltration with AN69 in ACEI-treated patients, under the present conditions, does not result in anaphylactoid reactions or in a clinically significant release of bradykinin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinin kinetics during different dialysis protocols with AN69 dialyser in ACEI-treated patients. 855 90


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