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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 5 (1978), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In urethane anaesthetized sham-operated rats, intravenous administration of Δ1-THC (1 mg/kg) caused an immediate and prolonged fall in blood pressure, with a concomitant reduction in pulse rate.2. In rats which had been adrenalectomized 24 h previously, Δ1-THC (1 mg/kg, i.v.) also caused a depressor response, but it was significantly shorter in duration than that observed in sham-operated animals. The durations of the cardiac slowing effect were similar in both groups of rats.3. Hydrocortisone pretreatment (25 μg/kg〉 i-v), given 45 min before Δ1-THC, restored the duration of the depressor response to Δ1-THC in adrenalectomized rats, but it did not have any effect on the bradycardia induced by Δ-THC.4. Hydrocortisone did not produce any significant effect on the hypotensive action of Δ1-THC in sham-operated rats, but the cardiac slowing effect was markedly potentiated.5. These results suggest a lack of correlation between the hypotensive and cardiac slowing actions of the drug and that a certein level of adrenal steroids is necessary for the maintenance of the depressor response to Δ1-THC.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 3 (1976), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Cardiovascular reflexes to intravenous adrenaline and histamine and to carotid occlusion were studied in the renal vasculature, and direct effects of nor-adrenaline and clonidine were compared in renal and hindlimb vascular beds in anaesthetized cats.2. Unlike its reported effects on cardiovascular reflexes in the hindlimbs, clonidine depressed all three reflexes in the kidneys.3. Noradrenaline caused vasoconstriction when given directly into both renal and hindlimb circulations, but clonidine produced vasoconstriction only in the hindlimb vascular bed.4. These results suggest that α-adrenoceptors in the renal vasculature may be different from those in the hindlimbs, and that the cardiovascular reflexes in these two areas are under different control.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 8 (1981), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: l. The depressor response, but not the cardiac slowing response, to the acute intravenous administration of Δ1-THC (1 mg/kg) was significantly reduced in urethane anaesthetized rats, which had been treated with daily injections of Δ1-THC (2 mg/kg, i.p.) for 10 days (P〈0.01).2. No significant differences in either the depressor or the negative chronotropic effects of an acute intravenous injection of Δ1-THC (1 mg/kg) were observed in anaesthetized rats which had been treated with PVP (8 mg/kg per day, i.p.) for 10 days.3. The depressor and cardiac slowing responses to an acute intravenous dose of Δ1-THC (1 mg/kg) were not significantly different between Δ1-THC- and PVP-treated animals which had been pithed.4. The potentiating effects of Δ1-THC on the pressor responses to intravenously administered noradrenaline were significantly reduced (P〈0.001) in urethane anaesthetized rats which had been treated with Δ1-THC, but not in anaesthetized PVP-treated animals.5. Tolerance to the potentiating effect of Δ1-THC on the responses to noradrenaline has also been demonstrated in anaesthetized Δ1-THC-treated rats, but not in pithed Δ1-THC treated ones.6. It is concluded that the development of tolerance to the depressor action of Δ1-THC, and its potentiating effect on the noradrenaline pressor responses requires the presence of an intact central nervous system.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 7 (1979), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Rat isolated hearts perfused with Δ1-THC (0·5 μ/ml) showed a reduction in the rate of beating which was not altered by pretreatment with propranolol (2 μg/ml), atropine (4 μg/ml) or hexamethonium (4 μ/ml).2. Propranolol (2 μg/ml) also caused a decrease in the rate of beating, which was not affected by pretreatment with Δ1-THC (0·5 μg/ml).3. In pithed rats, propranolol (2 mg/kg, i.v.) caused a decrease in the pulse rate, which was not altered by prior administration of Δ1-THC (1 mg/kg, i.v.).4. In both preparations, the responses to isoprenaline were markedly reduced or abolished by propranolol, but they were unaffected by Δ1-THC.5. It is concluded that the hypotensive and cardiac slowing actions of Δ1-THC are not mediated by activation of parasympathetic nerves or by β-adrenoceptor blockade.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 11 (1984), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Adrenaline 1 μg markedly elevated the activity of adenylate cyclase in ventricular tissue of rat hearts.2. Δ1-THC 25, 50 and 100 μg significantly reduced the adenylate cyclase activity with the maximum effect observed with the dose or 25 μg. Doses below or above this range did not produce any significant effect on the enzyme activity.3. Neither Δ6-THC 25 and 100 μg nor PVP 400 μg had any significant action on adenylate cyclase.4. The Δ1-THC-induced lowering of the cyclic AMP concentration in ventricular tissue of rat hearts can be explained, at least partly, by its ability to reduce the activity of adenylate cyclase in these tissues. It is suggested that this enzyme inhibition underlies the cardiac depressant action of Δ1-THC.
    Type of Medium: Electronic Resource
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