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31.
Angiotensinogen is thought to be an acute-phase protein, since its plasma concentrations increase in response to some inflammatory conditions, e.g. partial hepatectomy, nephrectomy or lipopolysaccharide (LPS) injection. However, this response of angiotensinogen has never been related to that of established acute-phase proteins. We have, therefore, examined plasma concentrations and hepatic secretion of angiotensinogen in two widely used inflammation models, i.e. turpentine or LPS injection in the rat, as well as in nephrectomized and sham-nephrectomized rats, in comparison to the response of two established acute-phase proteins, 1-acid glycoprotein (AGP) and 1-macroglobulin (AMG). Plasma concentrations and secretion rates of AGP and AMG increased significantly in all the conditions examined. The magnitude of the response decreased in the order turpentine > nephrectomy = LPS > sham nephrectomy. Angiotensinogen secretion was stimulated in LPS-injected (2.5-fold) and nephrectomized rats (2.6-fold), whereas no changes were seen in sham-nephrectomized rats. Surprisingly, a significant decrease both in secretion rates and plasma concentrations of angiotensinogen occurred in turpentine-injected rats.Intraperitoneal injection of interleukin 6, a major inductor of hepatic acute-phase proteins, increased plasma concentrations and hepatic secretion rates of AGP, AMG and angiotensinogen. Changes in liver angiotensinogen mRNA correlated well with angiotensinogen secretion rates in all groups, indicating that alterations in angiotensinogen synthesis are responsible for the observed changes in secretion rates and plasma concentrations. The response of angiotensinogen to turpentine is difficult to reconcile with the conventional definition of an acute-phase protein. 相似文献
32.
Transport of organic cations (OC) is important for the recycling of endogenous OC and also a necessary step for detoxification of exogenous OC in the body. Even though the identification and characterisation of numerous OC transporters in recent years has allowed the elucidation of molecular mechanisms underlying OC transport, elucidation of the regulation of this transport is just beginning. This review summarises the general properties of OC transport and then analyses the literature on the regulation of these processes. Studies on short- and long-term regulation of OC transport are considered separately. Important aspects of short-term regulation have been clarified and the regulatory pathways of several OC transporters have been characterised. Short-term regulation appears to be transporter subtype-, tissue- and species-dependent and to involve transporter phosphorylation. Transporter phosphorylation may alter the affinity for substrates or/and expression on the plasma membrane. Even though several studies have shown long-term regulation of OC transport, the pathophysiological meaning of these changes are not well understood. In this case, regulation seems to be subtype-, tissue- and gender-specific. Further research is necessary to clarify this important issue of regulation of OC transport. 相似文献
33.
The Bloom's Syndrome Registry was published in this journal in 1977. Now, in the first in a series of progress reports, recent accessions to the Registry are recorded, new instances of neoplasia are listed, and recent clinical observations and experimental results of general interest are cited. 相似文献
34.
Eberhard Schlatter 《Pflügers Archiv : European journal of physiology》1993,423(1-2):74-77
The tubuloglomerular feedback mechanism is inhibited by diuretics such as furosemide. For the macula densa (MD) cells similar transport systems, as present in thick ascending limb (TAL) cells, have been suggested. To examine this further, membrane voltages (V
m) of MD cells were recorded with the fast or slow wholecell patch-clamp method. The effects of diuretics on voltages and the conductance properties of these cells were examined. V
m of MD cells measured with the whole-cell patch-clamp method were as high as those in TAL cells: –72±1 mV (n=21). An increase in the extracellular K+ concentration by 15 mmol/l depolarized V
m of MD cells by 11±1 mV (n=18). Ba2+ (1 mmol/ l) reversibly depolarized MD cells by 10±2 mV (n= 10). Thus, MD cells possess a K+ conductance that could allow for the recycling of K+ taken up by the Na+-2 Cl–-K+ cotransporter. MD cells hyperpolarized reversibly upon addition of the loop diuretics furosemide, piretanide and torasemide, whereas muzolimine and hydrochlorothiazide, neither one acting on this cotransport system in other preparations including the TAL, had no effect on V
m. MD cells most likely possess the same cotransport system as the TAL cells, which drives NaCl reabsorption in the TAL and serves as sensor for the tubular NaCl concentration in MD cells. 相似文献
35.
Nikol S Maier A Krausz E Höfling B Huehns TY 《BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy》1998,9(5):375-388
No systemic pharmacological treatment has been convincingly shown to reduce the incidence of restenosis after angioplasty in patients. The lack of success of many pharmaceutical agents in reducing restenosis rates post-angioplasty and following stent implantation, as documented in dozens of clinical trials, has encouraged the development of new biotechnological approaches to the treatment of restenosis. Gene therapy and other agents, including antibodies, fusion toxins and ribozymes, have the potential to prevent some of the sequelae after arterial injury, particularly cell proliferation. Mechanical methods of preventing restenosis, for example sophisticated local drug delivery strategies and biodegradable stents using new materials, in combination with novel therapeutic agents or radiation, may also be of use. 相似文献
36.
Ilkka Pörsti Markus Hecker Eberhard Bassenge Rudi Busses 《Naunyn-Schmiedeberg's archives of pharmacology》1993,348(6):650-658
Summary We studied the functional role of angiotensin II (AII) receptor subtypes and vasodilatory endothelial autacoid release in response to AII in isolated perfused rabbit hearts. AII infusion induced biphasic changes in coronary perfusion pressure (CPP): an initial increase was followed by a decrease until a plateau was reached. At higher concentrations of AII (10 nmol/l) this plateau phase was lower than the initial CPP level. AII infusion elicited inverse changes in peak left ventricular pressure (LVP): coronary constriction was associated with a transient decline, and during the plateau phase LVP was clearly increased. AII also moderately augmented prostacyclin (PGI2) release from the coronary vascular bed. The AII-induced changes in CPP, LVP, and PGI2 release were effectively inhibited by the AT1 receptor subtype antagonist ICI D8731 (30 nmol/l), but not by the AT2 receptor antagonist CGP 42112 (30 nmol/l). The adenosine A1 receptor antagonist 8-phenyltheophylline (0.1 mol/l) attenuated the decline in CPP following the constriction phase without affecting the changes in LVP during AII infusion. The cyclooxygenase inhibitor diclofenac (1 mmol/l) had no effect on the AII-induced changes in CPP, whereas the nitric oxide-synthase inhibitor NG-nitro-L-arginine (30 mol/l) markedly potentiated the vasoconstriction but was without effect on the plateau phase of the response. In contrast to AII, the thromboxane analogue U46619 elicited sustained increases in CPP which were associated with slight decreases in LVP.In conclusion, AII induced a biphasic pressor response in the rabbit coronary vascular bed consisting of a transient vasoconstriction followed by a dilatation especially at higher concentrations of AII, an effect which was independent of the endothelial autacoids nitric oxide and PGI2. The AII-induced dilatation probably reflected rapid desensitization of the coronary arterial smooth muscle to the constrictor effect, and the concomitant accumulation of vasodilatory metabolites such as adenosine, generated during the positive inotropic action of AII. All the effects of AII in the rabbit heart appeared to be mediated via the AT, receptor subtype localized on coronary endothelial and smooth muscle cells, as well as on cardiomyocytes.On leave from the Department of Biomedical Sciences, University of Tampere, P.O. Box 607, FIN-33101 Tampere, FinlandCorrespondence to: I. Pörsti 相似文献
37.
Eberhard Schlicker Walter Schunack Manfred Göthert 《Naunyn-Schmiedeberg's archives of pharmacology》1990,342(5):497-501
Summary Discs of pig retina were preincubated with 3H-noradrenaline, 3H-dopamine or 3H-serotonin and then superfused. Electrical field stimulation increased the outflow of tritium from discs preincubated with 3H-noradrenaline or 3H-dopamine, but no from discs preincubated with 3H-serotonin. The tritium content at the end of superfusion was similar in discs preincubated with 3H-noradrenaline or 3H-dopamine but about tenfold lower in discs preincubated with 3H-serotonin. The tritium content in discs preincubated with 3H-noradrenaline was markedly reduced when desipramine was present during preincubation but was not affected by selective inhibitors of dopamine and serotonin uptake. The tritium content in discs preincubated with 3Hdopamine and 3H-serotonin, in contrast, was reduced or tended to be reduced by a selective dopamine and serotonin uptake inhibitor, respectively.The electrically evoked overflow of tritium from discs preincubated with 3H-noradrenaline was abolished by tetrodotoxin or omission of Ca2+. In discs superfused with desipramine, the electrically evoked overflow was enhanced by phentolamine but not affected by histamine. When both desipramine and phentolamine were present in the superfusion medium, histamine inhibited the evoked overflow (pIC15 6.85). This effect was mimicked by the histamine H3 receptor agonist R-(–)--methylhistamine as well as by its S-(+)-enantiomer (pIC15 7.85 and 5.30, respectively) but not by the H1 receptor agonist 2-(2-thiazolyl)ethylamine and the H2 receptor agonist dimaprit (each 10 mol/l). The inhibitory effect of histamine was abolished by the H3 receptor antagonist thioperamide 0.32 mol/l and attenuated by impromidine 3.2 mol/l but not affected by the H1 receptor antagonist dimetindene 3.2 mol/l and the H2 receptor antagonist ranitidine 10 mol/l.The results suggest that, in the pig retina, noradrenaline is taken up into, and released from, noradrenergic neurones (most likely vascular postganglionic sympathetic nerve fibres, less probably tissue-specific noradrenergic neurones of the retina) and that noradrenaline release is subject to modulation via H3 receptors and probably also a-adrenoceptors.Send offprint requests to E. Schlicker at the above address 相似文献
38.
Involvement of nitric oxide synthase in the physiology and pathophysiology of facial nerve function and dysfunction 总被引:1,自引:0,他引:1
O. Michel Alexander Hess Martin Krolzig Eberhard Stennert Klaus Addick Wilhelm Bloch 《European archives of oto-rhino-laryngology》2000,257(4):188-192
To date few reports have discussed the presence and function of nitric oxide (NO) in structures of the facial nerve. We performed
nicotinamide adenine dinucleotide phosphate (NADPH-d)-diaphorase-histochemistry and immunohistochemistry on the intratemporal
portion of the facial nerve, including the geniculate ganglion, of guinea pigs using specific antibodies to the three known
isoforms of NO synthase and soluble guanylyl-cyclase (sGC). Normal facial nerves were compared to those treated intratympanically
with bacterial lipopolysaccharides (LPS) and tumor necrosis factor-α (TNF-α). Both constitutive NOS isoforms and sGC could
be detected in the bipolar ganglion cells of normal animals, while the inducible isoform (iNOS or NOS II) was not found. Endothelial
NOS (NOS III) and sGC were present in blood vessels and were predominantly found in the perineurial sheath and less in the
endoneurium. sGC could be detected in all fibers in a cross section of the facial nerve. LPS and TNF treatment led to the
detection of iNOS in the perikaryia of the geniculate ganglion and the perineural sheath. These findings imply that NO may
be involved in neurotransmission at least in the visceroafferent system. NO regulates vascular tone of nutrient blood vessels
in the perineural sheath and endoneurium. The presence of sGC indicates that NO acts via its second messenger cGMP. NOS II
expression may be a contributing factor to facial nerve palsy via two different mechanisms: NOS II-generated NO may lead to
an overstimulation of the visceroefferent nerve fibers and motor fibers of the facial nerve. Dysregulation in facial nerve
blood vessels could lead to edema and elevated pressure on the nerve within its osseous canal.
Received: 13 April 1999 / Accepted: 12 August 1999 相似文献
39.
Hans Juha Exner Eberhard Schlicker 《Naunyn-Schmiedeberg's archives of pharmacology》1995,351(1):46-52
Mouse or rat brain cortex slices were preincubated with 3H-noradrenaline and superfused with physiological salt solution containing desipramine. We studied the effects of prostaglandin E2 (PGE2), prostaglandin D2 (PGD2) and related drugs on the electrically evoked (50 mA, 2 ms, 0.3 Hz) tritium overflow.PGE2 inhibited the electrically evoked tritium overflow from mouse brain cortex slices; the maximum effect of PGE2 (79010) was attenuated by the 2-adrenoceptor agonist talipexole (to 52010) and enhanced by the 2-adrenoceptor antagonist rauwolscine (to 92%). Rauwolscine was added to the superfusion medium in all subsequent experiments. The effect of PGE2 was readily reversible upon withdrawal from the medium and remained constant upon prolonged exposure of the tissue to the prostanoid. Studies with EP receptor agonists, mimicking the inhibitory effect of PGE2, showed the following potencies (pIC50): sulprostone (8.22); misoprostol (8.00); PGE2 (7.74); PGEZ (7.61); iloprost (5.86). The concentration-response curve of PGE2 was marginally shifted to the right by the EP1 receptor antagonist AH 6809 (6-isopropoxy-9-oxoxanthene-2-carboxylic acid; apparent pA2 3.97) and by the TP receptor antagonist vapiprost (4.50). AH 6809, by itself, did not affect the evoked overflow whereas vapiprost increased it. PGD2 inhibited the evoked overflow at high concentrations (pIC50 4.90); this effect was not altered by the DP receptor antagonist BW A868C (3-benzyl-5-(6-carboxyhexyl)-1-(2-cyclohexyl-2hydroxyethylamino)hydantoin), which, by itself, did not affect the evoked overflow. Indometacin slightly increased the evoked overflow and tended to increase the inhibitory effect of PGE2. PGE2 inhibited the electrically evoked tritium overflow also in rat brain cortex slices. The maximum effect (obtained in the presence of rauwolscine) was 61%; the pIC30 value was 7.67.The present study suggests that PGE2 inhibits noradrenaline release from mouse brain cortex via EP3 receptors and that its maximum effect is more marked in the mouse than in the rat. The inhibitory effect of PGD2 (in the mouse brain) does not involve DP receptors and may also be related to EP3 receptors. The EP3 receptors interact with a2-adrenoceptors and may be activated by endogenous prostanoids. 相似文献
40.