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  • 1995-1999  (1)
  • 1985-1989  (1)
  • PKC  (1)
  • lipid metabolism  (1)
  • 1
    Electronic Resource
    Electronic Resource
    The effects of prazosin and propranolol in combination with thiazide diuretics on blood pressure and serum lipids: a multicentre study (1987)
    Springer
    European journal of clinical pharmacology 33 (1987), S. 339-344 
    Details
    ISSN: 1432-1041
    Keywords: prazosin ; propranolol ; hypertension ; antihypertensive effects ; lipid metabolism ; multicentre study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary We have carried out randomized 12-week multicentre study to compare the effects of prazosin and propranolol on blood pressure and serum lipids in 70 patients with essential hypertension after a 4 week minimum period of treatment with thiazide diuretics. After 12 weeks treatment with prazosin (n=40, 1.5–12.0 mg per day) or propranolol (n=30, 30–120 mg per day) with diuretics there was a significant blood pressure reduction from 165.1/97.9 mmHg to 151.2/90.6 mmHg and from 167/96.5 mmHg to 153/91.9 mmHg, respectively. In the 12th week a significant decrease was noted in triglyceride and in low-density lipoprotein cholesterol (LDL + VLDL-C), but no significant effects were seen in high-density lipoprotein cholesterol (HDL-C) in patients receiving prazosin. On the other hand, a significant decrease in lecithin cholesterol acyltransferase (LCAT) was seen in patients receiving propranolol. Twenty-six of 40 patients receiving prazosin were given an additional 12 weeks of treatment. Twenty-two of 30 patients initially treated with propranolol were switched from propranolol to prazosin after 13 weeks and given prazosin up to the 24th week. At 24 weeks, the blood pressure was 149/93.0 mmHg in the prazosin group and 155/89.2 mmHg in the group which switched from propranolol to prazosin. Triglyceride remained reduced in the prazosin group at the 24th week. In the group which switched from propranolol to prazosin, triglyceride decreased significantly over the next 12 weeks.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00637627
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanisms of oxyradical production in substance P stimulated rheumatoid synovial cells (1996)
    Springer
    Rheumatology international 16 (1996), S. 159-167 
    Details
    ISSN: 1437-160X
    Keywords: Substance P ; Synovial cells ; Oxyradical production ; Intracellular Ca2+ ; PKC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the intracellular mechanisms of substance P induced oxyradical production in rheumatoid synovial cells by the luminol-dependent chemiluminescence method. After stimulation with substance P (30 μM), single synovial A (macrophage-like) or B (fibroblast-like) cells released oxyradicals such as superoxide anions (OZ) and/or hypochlorous anions (OCl−) under a microscope equipped with an ultrasensitive photonic image intensifier. The substance P induced oxyradical production was blocked by a tachykinin NK1 (NK1) receptor antagonist, GR82334, GTP-binding protein (G-protein) inactivators, GDPβS and islet-activating protein (IAP), and a phospholipase C (PLC) inhibitor, U-73122. Substance P (30 μM) also induced a transient increase in the intracellular Ca2+ concentration ([Ca2+]i) in both synovial A and B cells as measured by a Ca2+ indicator, fura 2. BAPTA-AM and an inositol-1,4-5-triphosphate (IP3) receptor antagonist, heparin, inhibited the substance P induced increase in [Ca2+]i, but they had no effects on oxyradical production. In contrast to the effects of BAPTA-AM and heparin, protein kinase C (PKC) inhibitors, H-7 and calphostin C, completely inhibited substance P induced oxyradical production without any significant effects on [Ca2+]i increase. These findings suggest that the NK1 receptor/PLC-linked diacylglycerol (DAG) formation with the resulting activation of PKC is the main signal transduction pathway for substance P stimulated oxyradical production in synovial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01419729
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    Paper (German National Licenses)
    Fulltext
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