Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Inhibitors of hepatic mixed function oxidase. 3. Inhibition of hepatic microsomal aniline hydroxylase and aminopyrine demethylase by 2,6- and 2,4-dihydroxyphenyl alkyl ketones and related compounds (1977)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 20 (1977), S. 1194-1199 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00219a017
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effects of 5,6-Dihydroxytryptamine on the Release, Synthesis, and Storage of Serotonin: Studies Using Rat Brain Synaptosomes (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 50 (1988), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 5,6-Dihydroxytryptamine is a neurotoxic analogue of serotonin which can have profound cardiovascular effects within minutes of administration in vivo (Korner and Head, 1981). These effects have been attributed to 5,6-dihydroxytryptamine-induced serotonin release, although there has been no biochemical assessment of the extent to which this occurs. The present study utilized an in vitro synaptosomal assay to determine the short-term effects of 5,6-dihydroxytryptamine on endogenous serotonin release, synthesis, storage, and metabolism. 5,6-Dihydroxytryptamine produced a rapid depletion of serotonin. At lower concentrations of 5,6-dihydroxytryptamine (0.1–1 μM), this depletion was associated primarily with an increase in the levels of 5-hydroxyindoleacetic acid, the deaminated metabolite of serotonin, with small increases in the amount of serotonin release. At higher concentrations (10–100 μM), a greater proportion of the depicted serotonin was released with less metabolism occurring. When metabolism was prevented by inhibiting monoamine oxidase, the amount of serotonin which was released equalled the amount of serotonin depletion. Thus monoamine oxidase activity was important in controlling the amount of serotonin which could be released by 5,6-dihydroxytryptamine. Further studies demonstrated that an impairment in serotonin synthesis and vesicular storage could account for the rapid depletion produced by 5,6-dihydroxytryptamine. Taken together, the results indicate that 5,6-dihydroxytryptamine acts to displace serotonin from vesicular stores into the cytoplasm where it can either be deaminated by monoamine oxidase or be released. Moreover, it is hypothesized that the intraneuronal concentration of 5,6-dihydroxytryptamine is important in determining the extent of serotonin release, because it can inhibit the deamination of serotonin by monoamine oxidase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1988.tb02944.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    VASCULAR REMODELLING AND MOLECULAR BIOLOGY: NEW CONCEPTS AND THERAPEUTIC POSSIBILITIES (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Over the past decade major advances in molecular cell biology have greatly increased our understanding of the way in which many growth factor genes are expressed and regulated. This knowledge is currently being translated into investigations of the cardiovascular system.2. Two growth factor families appear to play particularly important roles, the fibroblast growth factors and the transforming growth factors-β. These are multifunctional growth factors capable of remodelling the vasculature through their effects on cell migration, proliferation and matrix formation.3. An understanding of their regulation, properties and nature of their receptors is providing novel insights into the physiology and pathobiology of the vasculature. It is also providing highly specific targets for future therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb02742.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    REGULATION AND ROLE OF UROKINASE PLASMINOGEN ACTIVATOR IN VASCULAR REMODELLING (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Urokinase plasminogen activator (uPA) is produced and secreted by multiple vascular cell types, thus influencing the processes and the extent to which the vasculature is remodelled during the development of the intima or a neointima and during hypertrophy and angiogenesis.2. Urokinase plasminogen activator mRNA expression is up- and down-regulated by growth factors, cytokines and steroids. Urokinase plasminogen activator is secreted as a single chain inactive form that may be proteolytically converted to active or inactive forms. Targeting of proteolytic activity may occur via focalized expression of uPA and its cell surface receptors (uPAR). Proteolytic activity is also controlled through the often co-ordinated expression of specific inhibitors.3. A proteolytic cascade involving uPA provides its major role in tissue remodelling through the primary degradation of extracellular matrix and secondarily through the activation of transforming growth factor-β or release from the matrix of basic fibroblast growth factor. In addition, uPA secreted by growth factor-stimulated vascular cells may contribute to the chemotactic and mitogenic responses ascribed to the growth factor and recent evidence strongly suggests that uPA has direct biological actions on vascular cells.4. The cell surface binding of uPA via its growth factor-like domain to uPAR localizes and activates the protease, but may also initiate transmembrane signalling of biological responses, including migration/invasion and proliferation. As the uPAR lacks intracellular signalling domains, the signals may be transduced via interactions between uPA/uPAR and more classical signalling receptors. The mechanism by which uPA may be involved in cell signalling is yet to be elucidated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb01177.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    REGULATION BY PROTEIN KINASE C OF TRANSFORMING GROWTH FACTOR-β1 ACTION ON THE PROLIFERATION OF VASCULAR SMOOTH MUSCLE CELLS FROM SPONTANEOUSLY HYPERTENSIVE RATS (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. This study examined the role of protein kinase C (PKC) on the action of transforming growth factor-β1 (TGF-β1) to regulate the proliferation of vascular smooth muscle cells (VSMC) isolated from the aorta of the spontaneously hypertensive rat (SHR).2. Down-regulation of PKC by prolonged exposure to phorbol 12-myristate 13-acetate (PMA) completely inhibited the ability of TGF-β1 to potentiate epidermal growth factor-stimulated proliferation of VSMC.3. In contrast, the inhibitory effect of TGF-β1 on serumstimulated proliferation of VSMC was not altered by PMA action.4. These results suggest that PKC-dependent signalling pathways involved in the regulation of growth by TGF-β1 may be important in any proliferative component of vascular hypertrophy that develops in the SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb02783.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    RAT AORTIC SMOOTH MUSCLE CELLS EXPRESSING CHARYBDOTOXIN-SENSITIVE POTASSIUM CHANNELS EXHIBIT ENHANCED PROLIFERATIVE RESPONSES (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The relationship between the expression of potassium (K+) channels and the growth properties of cultured vascular smooth muscle cells was examined.2. Two groups of cells having different proliferative rates were cultured from the Wistar-Kyoto rat aorta. One group of cells, derived from early passages (3–3, proliferated with a cell doubling time of 2.41 days. A second group of cells, derived from late passages (〉 12), proliferated at a higher rate (cell doubling time, 0.61 days).3. Exposure of the early passaged cells to endothelin-1 (0.1 pmol/L) induced membrane depolarization. In contrast, exposure of the late passage cells to endothelin-1 (0.1 pmol/L) evoked a rapid hyperpolarization. The hyperpolarization in the late passage cells was blocked by charybdotoxin (20 nmol/L), an inhibitor of the large-conductance Calcium (Ca)-activated K+ channel.4. The authors conclude that rapidly proliferating vascular smooth muscle cells express enhanced activity of Ca-activated K+ channels causing marked alterations in the electrical properties of the cells. It is therefore suggested that the reported increase in Ca-activated K+ channel activity in the aortae of hypertensive rats is likely to be associated with the increased proliferative ability of the vascular smooth muscle cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02477.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    EFFECT OF TRANSFORMING GROWTH FACTOR-β1 ON PLATELET-DERIVED GROWTH FACTOR RECEPTOR BINDING AND GENE EXPRESSION IN VASCULAR SMOOTH MUSCLE CELLS FROM SHR AND WKY RATS (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. This study examined the effects of transforming growth factor-βl (TGF-β1) on platelet-derived growth factor-BB (PDGF-BB)-stimulated DNA synthesis, [125I]-PDGF-BB receptor binding and PDGF-β receptor mRNA expression in vascular smooth muscle cells (VSMC) isolated from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).2. TGF-β1 inhibited by 40% DNA synthesis stimulated by PDGF-BB in VSMC from WKY rats but potentiated by 20% growth factor-stimulated DNA synthesis in VSMC from the SHR.3. Since the difference in effect of TGF-β1 could not be attributed to differential regulation of [125I]-PDGF-BB binding activity and PDGF-β receptor mRNA expression, it is suggested that alterations in intracellular signalling pathways may account for the differential effects of TGF-β1 on PDGF-BB-stimulated DNA synthesis in VSMC from SHR and WKY rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02484.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    LONG-TERM ANGIOTENSIN II ANTAGONISM IN SPONTANEOUSLY HYPERTENSIVE RATS: EFFECTS ON BLOOD PRESSURE AND CARDIOVASCULAR AMPLIFIERS (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The angiotensin II type 1 receptor antagonist, losartan, prevented the development of hypertension in spontaneously hypertensive rats (SHR).2. Losartan also prevented the development of left ventricular hypertrophy and vascular amplifier abnormalities.3. Part of the hypotensive effect induced by long-term treatment with losartan persisted for a long time after the withdrawal of treatment.4. The results support the hypothesis that angiotensin II contributes to the development of hypertension and cardiovascular hypertrophy in SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00480.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    DIFFERENTIAL REGULATION BY TRANSFORMING GROWTH FACTOR-β1 OF PLATELET-DERIVED GROWTH FACTOR- STIMULATED PROLIFERATION OF VASCULAR SMOOTH MUSCLE CELLS FROM SHR AND WKY RATS (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. This study has examined and compared the time-course of action of transforming growth factor-β1 (TGF-β1) on platelet-derived growth factor-BB-stimulated proliferation of vascular smooth muscle cells isolated from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).2. Transforming growth factor-β1 inhibited vascular smooth muscle cell proliferation stimulated by platelet-derived growth factor-BB in WKY rats by approximately 60–75%.3. In contrast, transforming growth factor-β1 potentiated an 8–35% growth factor action on cell proliferation in the SHR.4. Defects in transforming growth factor-β1 action may be part of the molecular mechanism responsible for the development of vascular hypertrophy in the SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00481.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    SODIUM-DEPENDENT, ETHYLISOPROPYLAMILORIDE-SENSITIVE MECHANISMS REGULATE INTRACELLULAR pH IN HUMAN VASCULAR SMOOTH MUSCLE (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 17 (1990), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The pH-sensitive dye 2,7-biscarboxy-ethyl-5(6)-carboxyfluorescein (BCECF) was used to examine the contribution of Na+-H+ exchange and bicarbonate-dependent processes to intracellular pH (pHi) regulation in cultured human vascular smooth muscle.2. The recovery of pHi following an NH4Cl-induced acidosis was Na+-dependent and could be inhibited by ethylisopropylamiloride (200 μmol/L). Recovery was unaffected by the anion exchange inhibitor 4-acetamido-4′-isothio-cyano-stilbene-2,2′-disulfonic acid (200 μmol/L).3. Recovery from intracellular acidosis was more rapid when bicarbonate ions were present in the extracellular medium.4. The results suggest that Na+-H+ exchange as well as an Na+-dependent bicarbonate process, which can be inhibited by ethylisopropylamiloride, can influence the ability of smooth muscle to recover from intracellular acidosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1990.tb01324.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...