Drugs online research references
Brain Res. 1983 Oct 24;277(1):109-18.
The role of beta- and alpha-adrenoceptors in the regulation of the stages of the sleep-waking cycle in the cat.
Hilakivi I.
The effects of beta-adrenergic drugs alone and in combination with alpha-adrenergic drugs on the stages of the sleep-waking cycle were studied in adult cats. Polygraphic sleep recordings of 16 h showed that prenalterol (20 and 40 mg/kg i.p.), a beta 1-adrenoceptor-stimulating drug increased paradoxical sleep (PS) in a dose-related manner during 4-12 h. Salbutamol (40 mg/kg), a beta 2-adrenoceptor-stimulating drug, decreased PS during the first 4 h. Metoprolol (10 and 50 mg/kg), a relatively selective beta 1-adrenoceptor blocking drug, increased drowsy waking during the first 4 h. The larger dose also tended to decrease PS. Already at the lower dose metoprolol partially antagonized the PS increase produced by prazosin, an alpha 1-adrenoceptor blocking drug. Propranolol (5 mg/kg), a beta 1- and beta 2-adrenoceptor blocking drug, which alone decreases PS, antagonized the PS increase induced by phentolamine, an alpha 1- and alpha 2-adrenoceptor blocking drug. Atenolol (5 mg/kg), a poorly lipid-soluble beta-adrenoceptor blocking drug, failed to counteract phentolamine in increasing PS. Metoprolol (10 and 50 mg/kg) and propranolol (5 mg/kg) clearly potentiated the increase in drowsy waking and decrease in deep slow wave sleep and PS induced by clonidine (0.01 mg/kg), an alpha 2-adrenoceptor-stimulating drug. The results support the involvement of beta-adrenoceptors in the regulation of the sleep-waking cycle. A high level of beta-adrenergic activity may facilitate the production of PS. A low level of beta-adrenergic activity, especially in combination with a high level of alpha 2-adrenergic activity, may facilitate the production of drowsy waking. Central alpha 1- and beta 1-adrenoceptors may mediate opposite functions in the regulation of PS.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6315136&dopt=Abstract
Ter Arkh. 1993;65(4):40-3.
[The tourniquet test in evaluating the analgesic action of antianginal preparations]
[Article in Russian]
Zhiliaev EV, Glazunov AV.
Twenty-two patients with coronary heart disease (CHD) were examined for pain threshold and pain tolerance by a tourniquet test. The relationships between pain and ST segment depression were studied simultaneously during bicycle exercise. Pain sensitivity was measured in response to action of various antianginal drugs (isosorbide dinitrate, verapamil, nifedipine, diltiazem, propranolol, atenolol) and placebo. Reproducibility of the tourniquet test proved satisfactory. There were significant correlations between tourniquet test evidence and clinical patterns of ischemic myocardial episodes: significant differences in the values of pain threshold and pain tolerance in patients with painful myocardial ischemia, in combination of angina of effort with painless myocardial ischemia (p < 0.0001). Significant were also correlations between tourniquet test findings at bicycle exercise and value describing the proportion of ST depression to pain. As for the drugs, verapamil appeared most active in the tourniquet test (p < 0.02 and p < 0.05 for pain threshold and pain tolerance, respectively). Pain tolerance changes due to isosorbide dinitrate were somewhat greater than for placebo (p = 0.06). The study provided evidence in support of the adequacy of the tourniquet test for assessment of general pain sensitivity and pain sensitivity to myocardial ischemia as well as of analgetic effects of the drugs. Verapamil and isosorbide dinitrate are suggested to have analgetic activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8059406&dopt=Abstract
J Clin Endocrinol Metab. 1992 Feb;74(2):441-6.
Differential changes in alpha- and beta-adrenoceptor linked [45Ca2+] uptake in platelets from patients with anorexia nervosa.
Gill J, DeSouza V, Wakeling A, Dandona P, Jeremy JY.
Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine, London, England.
[45Ca2+] Uptake was studied in response to adrenaline, isoprenaline, noradrenaline, and (Bu)2cAMP in platelets from patients with anorexia nervosa. In both controls and anorectics, adrenaline, isoprenaline, noradrenaline, and (Bu)2cAMP stimulated [45Ca2+] uptake. In receptor subtype characterisation studies on control platelets, adrenaline-stimulated [45Ca2+] uptake was blocked by yohimbine (an alpha 2-adrenoceptor antagonist) and the specific beta 2-adrenoceptor antagonist ICI 118,551, but not by atenolol (a beta 1-antagonist). Isoprenaline action was blocked by ICI 118,551, but not by yohimbine. Noradrenaline-stimulated [45Ca2+] uptake was blocked by yohimbine but not by ICI 118,551. In platelets from anorectic patients, there was a significant increase in noradrenaline-stimulated [45Ca2+] uptake, a significant diminution in adrenaline and isoprenaline-stimulated [45Ca2+] uptake, but no significant difference in (Bu)2cAMP-stimulated [45Ca2+] uptake, when compared with controls. Basal uptake was also significantly enhanced in anorectics and was found to be inhibited with verapamil but not adrenoceptor antagonist. These data firstly indicate that both alpha 2- and beta 2-adrenoceptor activation elicits [45Ca2+] uptake by platelets. It is proposed that this stimulated [45Ca2+] uptake does not reflect changes in cytosolic Ca2+ but to localized changes of Ca2+ at the plasma membrane, possibly associated with receptor activation, per se. The respective increase and decrease of alpha- and beta-adrenoceptor activity in platelets from anorectic patients is in accord with other reports of changes of adrenoceptor number and type in platelets and other cells from anorectic patients. There may also be an increase in calcium channel activity in platelets from anorectics.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1346146&dopt=Abstract
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