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  • 1
    ISSN: 0022-4731
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of pineal research 5 (1988), S. 0 
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Some data from the literature raised the possibility of an interaction between the opioidergic system and pineal secretion. The present study was undertaken in order to investigate the acute influence exerted by opioids upon plasma melatonin levels in the albino rat. Different doses of morphine hydrocloride were injected (1, 1.5, 2, 3 mg/kg) intraperitoneally into anaesthetized adult male rats bearing a cannula previously inserted into the carotid. Blood samples were collected subsequently at 30-min intervals, within a period of 90 min following drug administration. Plasma melatonin contents were determined by a radioimmu-noassay (RIA) method. Acute administration resulted in a dose-dependent increase in plasma melatonin concentration when compared to the respective controls. This effect is blocked by pretreatment with Naloxone. The present result seem to support the hypothesis that the opioidergic system, in certain circumstances, might contribute to the activation of melatonin secretion.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of pineal research 17 (1994), S. 0 
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Esposti D, Mariani M, Demartini G, Lucini V, Fraschini F, Mancia M. Modulation of melatonin secretion by acetyl-L-carnitine in adult and old rats. J. Pineal Res. 1994; 17: 132–136.Abstract; Modification of melatonin synthesis and release by acetyl-L-carnitine (ALC) was studied in adult (2 month old) and old (24-month-old) male Sprague Dawley rats. When ALC was injected at 1500 into adult rats at doses of 10, 30, or 90 mg/kg, there was a remarkable increase in their pineal and serum melatonin 1 hr later. However, using the same experimental protocol acute ALC administration in old rats did not modify pineal and serum melatonin levels. ALC administered in the same dose range induced a significant increase in pineal and serum melatonin in adult rats treated at 0100 h following exposure of 30 min to bright, white light to suppress endogenous melatonin. In the same conditions, in old rats, only the higher dose (90 mg/kg) caused any noteworthy increase in melatonin pineal content while lower doses were ineffective both on serum and pineal melatonin levels. It is known that ALC affects fatty acid transport in the cells, modulates Co A, modifies neuronal transmission and reduces lipofuscin accumulation which is related to lipid per oxidation. The action of ALC on melatonin synthesis could be the result of a modulation of the neuronal transmission related to circadian pineal endocrine activity. Moreover, since both ALC and melatonin exert remarkable scavenger activity, it is possible to suppose that ALC effects in reversing certain aging processing may be due to its ability to promote melatonin production.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1435-1463
    Keywords: Opioid system ; melatonin ; pineal gland
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent reports point to a link between the pineal gland and the opioid system. In order to investigate this relationship, two separate studies were performed on humans. Beta-endorphin plasma levels were determined after melatonin administration (0.2 mg/kg b.w. i.m. at 2 p.m.). Melatonin serum values were evaluated after administration of FK 33-824, a met-enkephalin analogue (0.3 mg i.v. infusion at 9 a.m.). A significant decrease of beta-endorphin plasma levels was observed 120 minutes after melatonin injection. Melatonin release was stimulated by FK 33-824, with a peak at 30 minutes. The present results provide evidence of the inhibitory effect of melatonin on beta-endorphin secretion and the stimulatory action of the opioid peptides on the pineal gland. However, further studies will be required to clarify the relationship between the opioid system and the pineal gland.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    European journal of epidemiology 8 (1992), S. 129-133 
    ISSN: 1573-7284
    Keywords: ACE-inhibitors ; Atherosclerosis ; Blood vessels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The involvement of the circulating and local renin-angiotensin system in atherosclerotic process has been hypothesized on the basis of experimental data showing presence and specific actions of the components of this system in the vascular wall. In particular, angiotensin II may participate in well known events in atherogenesis as the control of smooth muscle cell growth and proliferation. Recent studies have shown an effect of angiotensin converting enzyme (ACE) inhibition on the development of atherosclerosis in animal models. Captopril and cilazapril prevent myointimal proliferation after vascular injury in rat. Captopril reduces aortic cholesterol content and percentage intmal aortic surface covered by lesions in Watanabe heritable hyperlipidemic rabbits. Captopril also significantly reduces the progression of carotid and coronary lesions in monkeys fed a high cholesterol diet. In addition, a role for converting enzyme inhibitors in reducing aortic and microvascular growth either in hypertensive or normotensive rats has been demonstrated. It is possible that ACE-inhibitors prevent angiotensin II-induced vascular proliferation and thereby suppress the development of atherosclerosis in animals. It is also conceivable that the blood pressure effects of ACE-inhibitors could play a role in the antiatherosclerotic effect shown by these drugs, even though this explanation cannot be addressed by studies dealing with normotensive animals. Then, other mechanisms could be involved, including hypothesized effects of blockade of the renin-angiotensin system on sympathetic nervous system activity, regulation of vascular growth factors and insulin sensivity. The clinical significance of these experimental findings is unknown. Molecular mechanisms by which the renin-angiotensin system can act on atherosclerosis pathogenesis and the influence of ACE-inhibitors on the course of arterial diseases in humans ought to be important subjects of future investigations.
    Type of Medium: Electronic Resource
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