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  • 1990-1994  (3)
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  • 1
    Electronic Resource
    Electronic Resource
    MECHANISMS INVOLVED IN THE STIMULATION OF ALDOSTERONE PRODUCTION BY ANGIOTENSIN II, VASOPRESSIN AND ENDOTHELIN (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. Endothelin (ET), vasopressin (VP) and angiotensin II (AII) all stimulate aldosterone production in adrenal glomerulosa cells but the response to AII is greater than that to either ET or VP.2. Total inositol phosphate responses to AII and ET were similar but the response to VP was lower.3. Cytosolic free Ca2+ responses to AII were higher than to either of the other peptides.4. Metabolism of 145IP3 was different under stimulation by the three different peptides.5. Adrenal glomerulosa cells can distinguish between three different agonists which stimulate phosphatidylinositol turnover and produce a selective response to each peptide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1990.tb01318.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    IONIC MECHANISMS REGULATING SODIUM ENTRY INTO VASCULAR SMOOTH MUSCLE (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Na+/H+ exchange, an ethylisopropylamiloride (EIPA)-sensitive Na+ and HCO3- dependent system and a diisothio-cyanatostilbenedisulphonic acid (DIDS)-sensitive Na+ and HCO3- transporter, contribute to sodium influx and intracellular pH (pHi) regulation in vascular smooth muscle.2. In cultured cells from the human internal mammary artery, Na+/H+ exchange and the EIPA-sensitive Na+ and HCO3- dependent system contribute about 80% to basal sodium influx. The residual Na+ influx is both EIPA and DIDS-insensitive.3. Sodium influx via these mechanisms influences the ability of vascular smooth muscle to synthesize protein late in the G1 phase of the mitotic cell cycle. This, in turn, affects DNA biosysthesis.4. These Na+ exchanges/transporters have the capability to facilitate the development of vascular hypertrophy in hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1991.tb01419.x
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    Paper (German National Licenses)
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  • 3
    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
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    Paper (German National Licenses)
    Fulltext
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