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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 90-92 
    ISSN: 1432-1440
    Keywords: Nicotine and metabolites ; Dose-response curves ; Blood pressure ; Heart rate ; Anaesthetized rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Blood pressure and heart rate in anaesthetized rats has been determined after i.v. injection of increasing doses of nicotine (NI) and its major metabolites, i.e. continine (CO), nornicotine (NOR), metanicotine (MN) and dihydrometanicotine (DMN). NI and MN elicited similar dose response curves, increasing blood pressure according to the dose injected. However, the dose response curve of MN was shifted to the right. Furthermore DMN caused similar pressor effects than MN and the pressor effects of NOR was even weaker. Only after injection of CO was a dose-dependent depressor effect observed and this was reversed after very high doses. CO also reduced heart rate in a dose-dependent manner, whereas NI and its other metabolites did not significantly change heart rate.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 35 (1988), S. 53-57 
    ISSN: 1432-1041
    Keywords: codergocrine ; prolactin ; hydergine ; pharmacokinetics ; systemic availability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary We have studied the absolute systemic availability (f) of an oral formulation (Hydergin spezial = Hydergine FASR 4 mg per tablet) of codergocrine by three different methods. Twelve healthy volunteers received single doses of 0.9 mg co-dergocrine intravenously and 8.0 mg orally in a randomized crossover design. The pharmacological effect of co-dergocrine was monitored as a reduction in plasma prolactin. Maximal plasma concentrations of co-dergocrine after oral dosing ranged between 0.181 and 1.307 ng·ml−1. Maximal urinary excretion ranged between 4.7 and 9.9 µg·h−1 and between 0.3 and 2.3 µg·h−1 after intravenous and oral doses respectively. Clearance was measured as 90±22 l·h−1 and the absolute systemic availability (f) as 2.25±0.65% by using the areas under the plasma concentration-time curves extrapolated to infinity. Calculation of f by comparing areas up to 32 h or the fractions of the dose excreted in urine led to identical results. The intravenous and oral doses produced similar pharmacological effects (reduction of plasma prolactin concentrations) despite the small value of f.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 763 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 763 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0167-0115
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 16 (1984), S. 26 
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 93 (1998), S. s024 
    ISSN: 1435-1803
    Keywords: Key words Renin-angiotensin system (RAS) – sympathetic system – angiotensin II – noradrenaline and adrenaline release – ACE inhibitors – AT1 receptor antagonists – bradykinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Angiotensin II is able to modulate both the presynaptic sympathetic system and the adrenal medulla resulting in an enhanced release of noradrenaline and adrenaline. Consequently, the inhibition of the converting enzyme by ACE inhibitors resulting in a lower concentration of angiotensin II or blockade of the specific AT1 receptors by AT1 receptor blocking agents should lead to a decrease in both noradrenaline and adrenaline release. It has been demonstrated that ACE inhibition did not influence the net catecholamine overflow during stimulation of the sympathetic nerves in contrast to AT1 antagonists which can specifically and dose dependently diminish noradrenaline and adrenaline release, an effect that could be explained by a compensating mechanism of bradykinin. Bradykinin may accumulate during ACE inhibition and is able to stimulate catecholamine release via B2 receptors. To verify the class effect of AT1 antagonists on presynaptic AT1 receptors, the AT1 antagonist candesartan was investigated regarding its presynaptic effect in pithed spontaneously hypertensive rats. As could be demonstrated with losartan and HR 720, candesartan lowered AT1 receptor mediated angiotensin II-induced noradrenaline release in a dose-dependent manner. It is concluded that AT1 antagonists inhibit angiotensin II mediated catecholamine release on presynaptic sympathetic nerves and the adrenal medulla at the specific AT1 receptor site. The effect can be described as a class effect of these imidazole derivatives.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1440
    Keywords: Cardiac transplantation ; Plasma renin activity ; Atrial natriuretic factor ; Cyclic guanosine monophosphate ; Plasma catecholamines ; Arterial hypertension ; Exercise testing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of graded supine ergometry on blood pressure, heart rate, and plasma hormones were studied in 14 hypertensive heart transplant recipients before and after 2 weeks and 6 months of enlapril (20 mg/day) plus furosemide (20–80 mg/day) alone or combined with verapamil (120–360 mg/day). Each time, measurements were obtained at rest and at 25 and 50 W exercise. Anti-hypertensive therapy normalized blood pressure, while heart rate and the blood pressure response to exercise remained unaltered. Pretreatment resting plasma renin activity and catecholamine levels were normal, while atrial natriuretic factor and cyclic guanosine monophosphate concentrations were elevated. All hormones increased significantly with exercise. During treatment, plasma renin activity increased and atrial natriuretic factor and cyclic guanosine monosphosphate levels decreased significantly, with a blunted exercise response; concentration of catecholamines increased significantly, with augmented exercise response. Thus, the chosen regimen allowed effective, lasting BP control in hypertensive transplant patients but was associated with significant changes in plasma hormones. Whereas the rise in plasma renin activity may be attributed to converting enzyme inhibition, the decreases in atrial natriuretic factor and cyclic guanosine monophosphate and increases in catecholamine levels seem to indicate marked changes in resting and particularly exercise hemodynamics during antihypertensive therapy.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 31-35 
    ISSN: 1432-1912
    Keywords: Brain microdialysis ; Anterior hypothalamus ; Catecholamine release ; Angiotensin II ; Dopamine metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microdialysis was used to investigate whether angiotensin II modulates the basal and K+-induced release of endogenous noradrenaline, dopamine and their metabolites 3,4-dihydroxyphenylglycol (DOPEG) and 3,4-dihydroxyphenylacetic acid (DOPAC) from the anterior hypothalamus of the anaesthetized rat. The release of the amines was stimulated twice (ST1 and ST2) with either 50 mmol/l or 100 mmol/l K+. The release of each amine induced by K+ was reproducible and concentration-dependent. Angiotensin II when present in the perfusion fluid after ST1 at a concentration of 0.1 and 10 μmol/l (chosen after in vitro experiments had shown that the recovery of the peptide across the dialysis membrane was only 3.6%), had no significant effect on amine release. However, 10 μmol/l angiotensin II induced an immediate, significant increase in basal DOPAC outflow which reached a maximum of 89% in the 100 mmol/l K+ and 53% in the 50 mmol/l K+ experiments. No such effect was observed with DOPEG outflow. In a separate experimental series, addition of angiotensin II without a preceding K+ stimulation period did not significantly affect the outflow of the amines and metabolites. The results suggest that angiotensin II can selectively influence dopamine metabolism in the anterior hypothalamus in vivo but does not act locally to acutely facilitate the release of endogenous catecholamines from this brain area.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1912
    Keywords: Brain microdialysis ; Anterior hypothalamus ; Noradrenaline ; Dopamine ; 3,4-Dihydroxyphenylglycol ; 3,4-Dihydroxyphenylacetic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The novel technique of microdialysis has been used to examine the basal and K+-induced release of catecholamines and metabolites from the anterior hypothalamus of the urethane-anaesthetized rat in vivo. A high pressure liquid chromatographic assay was developed to simultaneously measure endogenous noradrenaline, dopamine and their intraneuronal metabolites 3,4-dihydroxyphenylglycol (DOPEG) and 3,4-dihydroxyphenylacetic acid (DOPAC) respectively, in each 60 μl dialysate sample. The effect of replacing Ca2+ in the perfusion fluid with a low concentration of Cd2+, which blocks Ca2+ effects, was also studied. Increasing the K+ concentration in the perfusion fluid elicited a concentration-dependent increase in noradrenaline and dopamine release. In contrast, there were marked reductions in DOPEG and DOPAC which were not concentration-dependent. In the Ca2+-depleted conditions, the K+-induced increase in amine release was significantly attenuated, but the reductions in the metabolites were not affected. We suggest that the mechanisms contributing to the observed reductions in the metabolites may be inhibition of neuronal reuptake, an increase in neuronal efflux, an enhancement of vesicular uptake and a decrease in vesicular efflux.
    Type of Medium: Electronic Resource
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