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  • 1
    Electronic Resource
    Electronic Resource
    POTENTIATION OF DEPRESSOR RESPONSES TO ARACHIDONIC ACID BY ANGIOTENSIN CONVERTING ENZYME INHIBITORS IN THE RAT (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 11 (1984), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In chloralose anaesthetized rats, intravenous administration of captopril, SQ 20881, SA 446 or MK 421 (0.5 mg/kg) potentiated the depressor responses to arachidonic acid 3 mg/kg given intravenously.2. Same doses of the above angiotensin converting enzyme inhibitors caused an approximately 100-fold decrease in sensitivity to the pressor effects of angiotensin I, with a concomitant similar increase in sensitivity to the depressor effects of bradykinin.3. Depressor responses to arachidonic acid, both before and after administering the converting enzyme inhibitors, were abolished by intravenous indomethacin (5 mg/kg).4. These results suggest that increased synthesis of prostaglandins in the circulation may contribute to the hypotensive effect of the angiotensin converting enzyme inhibitors, a group of newly developed antihypertensive agents.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1984.tb00875.x
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  • 2
    Electronic Resource
    Electronic Resource
    CAPTOPRIL DOES NOT POTENTIATE HYPOTENSION AND ALGESIA BY SUBSTANCE P (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 13 (1986), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Captopril (1–5 mg/kg, i.v.) did not affect the vasodepressor responses to substance P (1–30 μg/kg, i.v.) in anaesthetized rats.2. Substance P (100 μg/kg, s.c.) produced significant algesia in mice; this was not potentiated by the smaller doses of captopril (1–2 mg/kg, i.p.), but was instead antagonized by the high dose (5 mg/kg, i.p.).3. It is concluded that captopril does not have any influence on substance P degradation in vivo since the pharmacological actions of the undecapeptide are not enhanced after captopril treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1986.tb02386.x
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  • 3
    Electronic Resource
    Electronic Resource
    MECHANISMS OF CAPTOPRIL-INDUCED POTENTIATION OF THE DEPRESSOR RESPONSES TO ARACHIDONIC ACID IN RATS (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 13 (1986), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The mechanisms underlying potentiation by captopril of the depressor responses to arachidonic acid were studied in chloralose-anaesthetized rats.2. Captopril, in a dose (0.5 mg/kg, i.v.) which inhibited the pressor responses to angiotensin I (0.03-1 μg/kg, i.v.), enhanced the depressor responses to bradykinin (3-300 μg/kg, i.v.) and potentiated the hypotensive action of arachidonic acid (3 mg/kg, intravenously). This phenomenon was observed not only when captopril and arachidonic acid were administered intravenously, but also when these compounds were injected directly into the aortic arch.3. The enhancement of arachidonic acid-induced hypotension by captopril was not significantly affected by pretreatment with a low dose of aprotinin (3 mg/kg, i.v.), but was abolished by bilateral nephrectomy or by pretreatment with a higher dose of aprotinin (6 mg/kg, i.v.).4. It is suggested that captopril augments the depressor responses to arachidonic acid by inhibiting angiotensin converting enzyme. This results in accumulation of bradykinin which in turn increases release of vasodilator prostaglandins, originating most probably, from the kidneys. The possibility that blockade of angiotensin II formation by captopril may leave the vasodilator action of prostaglandin unopposed cannot be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1986.tb00325.x
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  • 4
    Electronic Resource
    Electronic Resource
    ARACHIDONIC ACID METABOLISM IN NICOTINE-TREATED RATS AND NICOTINE-INCUBATED RABBIT AORTIC SMOOTH MUSCLE CELLS (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 changes in plasma levels of thromboxane-B2 (TXB2) and 6-keto-prostaglandin-F1α(6-keto-PGF1α) were examined in rats given 5, 25, 50 or 100 μg/mL nicotine in drinking water for 10 days.2. The effect of nicotine on prostacyclin (PGI2) synthesis from endogenous arachidonic acid by cultured rabbit aortic smooth muscle cells was also studied.3. Plasma levels of TXB2 were increased dose-dependently by treatment for 10 days with nicotine.4. 6-Keto-PGF1α values were lowered dose-dependently, both in the plasma of nicotine-treated rats and in rabbit aortic smooth muscle cells incubated with the alkaloid.5. The results suggest that endogenous synthesis of thromboxane-A2 and PGI2, as reflected by TXB2 and 6-keto-PGF1α levels, respectively, is influenced by nicotine treatment. These findings may be related to cardiovascular diseases associated with cigarette smoking, but further studies are needed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00405.x
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  • 5
    Electronic Resource
    Electronic Resource
    Low Frequency Sound and Oxytocic Activity of Plasma in Rats (1967)
    [s.l.] : Nature Publishing Group
    Nature 214 (1967), S. 1112-1113 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Oxytocic activity in plasma has now been measured in rats, some of which were exposed and some not exposed to 150 c/s, and also it has been measured 30 and 60 min after subcutaneous administration of oxytocin (4 and 20 mil/animal). Water loading and auditory excitation were carried out as before1. ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/2141112a0
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    A comparative study of the gastric ulcerogenic effects of stress and reserpine in rats with decreased stomach wall mast cell populations (1980)
    Springer
    Cellular and molecular life sciences 36 (1980), S. 995-996 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Stress-induced gastric glandular ulcers in rats appeared less severe than those evoked by reserpine, although glandular mucosal mast cell counts were equally decreased. Prior depletion of the glandular mucosal mast cell population confirmed the hypothesis that an additional mechanism contributes to reserpine ulceration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01953842
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  • 7
    Electronic Resource
    Electronic Resource
    The influence of chronic nicotine treatment on stress-induced gastric ulceration and emptying rate in rats (1992)
    Springer
    Cellular and molecular life sciences 48 (1992), S. 389-391 
    Details
    ISSN: 1420-9071
    Keywords: Nicotine ; cold-restraint stress ; gastric ulcers and motility
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Ten-day treatment with nicotine, (5, 25 or 50 μg/ml drinking water) dose-dependently intensified gastric ulceration induced by cold-restraint, and emptying rate. Stomach contractions produced by graded doses of bethanechol i.v. were elevated further by nicotine treatment. It is suggested that chronic nicotine administration produces hypersensitivity of the gastric muscarinic receptors; stomach hypermotility contributes to the ulcer-worsening action of the alkaloid
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01923437
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  • 8
    Electronic Resource
    Electronic Resource
    Nitric oxide inhibition intensifies cold-restraint induced gastric ulcers in rats (1993)
    Springer
    Cellular and molecular life sciences 49 (1993), S. 304-307 
    Details
    ISSN: 1420-9071
    Keywords: NW-nitro-l-arginine methyl ester ; nitric oxide ; cold-restraint stress ; mucosal ulcers ; mast cells ; rat stomachs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Treatment 20 min beforehand with an inhibitor of nitric oxide (NO) synthesis, NW-nitro-l-arginine methyl ester (L-NAME) (12.5, 25, 50 or 100 mg/kg, s.c.), dose-dependently intensified gastric glandular mucosal ulceration produced by cold-restraint stress. Hexamethonium (20 mg/kg) or atropine (1 mg/kg) pretreatment s.c. 20 min before stress strongly antagonised stress-evoked ulceration, as well as the ulcer-potentiating effects of L-NAME when either cholinoceptor antagonist was given concurrently with the NO inhibitor. Stress-induced mast cell degranulation was not worsened by L-NAME pretreatment. The findings suggest that NO could confer partial protection against stress-induced gastric ulcer formation; its activity is triggered off by the ulcerogenic mechanism of stress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01923407
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  • 9
    Electronic Resource
    Electronic Resource
    The effect of nicotine on ethanol-induced gastric ulcers in rats (1985)
    Springer
    Cellular and molecular life sciences 41 (1985), S. 1140-1141 
    Details
    ISSN: 1420-9071
    Keywords: Nicotine ; ethanol ; gastric ulcers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Nicotine, in concentrations of 5 and 25 μg/ml drinking water, given ad libitum for 10 days, dose-dependently increased lesion formation and worsened ethanol-induced ulceration in rat stomachs. Daily fluid intake and b.wt gain were not adversely affected by nicotine pretreatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01951697
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  • 10
    Electronic Resource
    Electronic Resource
    N-ethylmaleimide antagonizes stress-induced gastric ulcers in rats (1991)
    Springer
    Cellular and molecular life sciences 47 (1991), S. 250-251 
    Details
    ISSN: 1420-9071
    Keywords: N-ethylmaleimide ; cold-restraint gastric ulcers ; sulfhydryl substances
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary N-ethylmaleimide (NEM) 10 or 25 mg/kg b.wt, given s.c. 20 min beforehand, dose-dependently and significantly antagonizes the severity of gastric glandular ulcers produced by restraint at 4°C (stress) for 2 h. These findings suggest that reduced activity of endogenous nonprotein sulfhydryl substances in gastric tissue does not worsen stress-induced ulceration in rat stomachs, unlike the deleterious effect its depletion is claimed to have on ethanol-evoked gastric mucosal damage. Thus, decreased SH activity appears not to play a role in the aetiology of mucosal ulcers due to stress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01958150
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