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  • 1
    Electronic Resource
    Electronic Resource
    Second Messengers Are Involved in Facilitatory but Not Inhibitory Receptor Actions at Sympathetic Nerve Endings (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 604 (1990), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1990.tb31999.x
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  • 2
    Electronic Resource
    Electronic Resource
    ADRENALINE AND STRESS-INDUCED INCREASES IN BLOOD PRESSURE 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. Stress was induced by immobilizing the hind limbs of rats for 12 days and housing the rats in individual cages. Control rats were housed in groups without immobilization. Blood pressure and heart rate were measured through an indwelling carotid cannula.2. After 10 and 12 days of immobilization and isolation, the stressed rats had significantly higher blood pressures (ca. 10 mmHg) and higher cardiac adrenaline levels (ca. 90%). After adrenal medullectomy cardiac adrenaline levels were markedly reduced in both stressed and control rats. Furthermore, the stressing procedure did not cause a rise in blood pressure in adrenal-medullectomized rats.3. Desipramine HCl (2 mg/kg per day), administered orally to block the neuronal uptake of adrenaline, prevented the elevation in blood pressures and cardiac adrenaline levels. Propranolol HCl (2.8 mg/kg per day), orally, also prevented the rise in blood pressure.4. The results are consistent with the hypothesis that activation of facilitatory prejunctional β-adrenoceptors on sympathetic nerves by neuronally-released adrenaline may be responsible for the raised blood pressure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1986.tb00349.x
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  • 3
    Electronic Resource
    Electronic Resource
    HYPERTENSION THROUGH ADRENALINE ACTIVATION OF PREJUNCTIONAL β-ADRENOCEPTORS (1981)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 8 (1981), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Adrenaline can enhance the stimulation-induced release of transmitter noradrenaline in sympathetically innervated tissues by activating prejunctional β-adrenoceptors.2. Adrenaline incorporated into sympathetic transmitter stores by neuronal uptake can be subsequently released as a co-transmitter and can then activate prejunctional β-adrenoceptors, thus completing a facilitatory feedback loop.3. Rats chronically treated with adrenaline develop elevated blood pressures compared to control rats, β-adrenoceptor blockade prevents the rise in blood pressure.4. Activation by adrenaline of facilitatory prejunctional β-adrenoceptors of sympathetic nerves innervating cardiovascular effector tissues may explain adrenaline-induced rises in blood pressure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1981.tb00750.x
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  • 4
    Electronic Resource
    Electronic Resource
    PROTEIN KINASE C AND TRANSMITTER RELEASE (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Protein kinase C (PKC) is an important second messenger-activated enzyme. In noradrenergic nerves it appears to be tonically activated by diacylglycerol (DAG) to facilitate transmitter release and the steps in this involve activation of phospholipase C, generation of DAG and activation of PKC. It is suggested that the subsequent facilitation of transmitter release is due to the phosphorylation of proteins involved in the release process distal to Ca2+entry, presumably those involved in vesicle dynamics.2. There are differences between central noradrenergic neurons and sympathetic nerves. In central neurons PKC appears to be tonically active and its inhibition results in a decrease in noradrenaline release under most, if not all, conditions.3. In sympathetic nerves PKC inhibitors only decrease transmitter release during high-frequency stimulation and not during low-frequency stimulation. At high frequency there is a gradual increase in the effect of PKC inhibitors on transmitter release during the first 15 s of a stimulation train. It is suggested that this is due to a progressive rise in intracellular Ca2+ and a consequent activation of PKC.4. Activation of PKC by phorbol esters produces a large enhancement in action potential-evoked noradrenaline release in both the central nervous system and in peripheral tissues. The structural requirements of the phorbol esters for maximal effect suggest that the phorbol esters must access the interior of the nerve terminal to activate PKC and the neural membrane acts as a barrier for highly lipophilic phorbol esters, thereby reducing their activity. Activation of PKC represents one of the most powerful ways to enhance transmitter release and may have therapeutic potential.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1997.tb02102.x
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  • 5
    Electronic Resource
    Electronic Resource
    17β-OESTRADIOL ENHANCES NITRIC OXIDE SYNTHASE ACTIVITY IN ENDOTHELIUM-DENUDED RAT AORTA (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 25 (1998), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. It has been suggested that oestrogen-produced vasodilatation is due to induction of endothelial nitric oxide synthase (NOS), but there are many reports of direct effects on vascular smooth muscle. In the present study, these processes were investigated in rat aorta isolated from ovariectomized rats.2. Short-term treatment (10min) with 17β-oestradiol (10 μmol/L) produced a small attenuation of the phenylephrine (PE)-induced constriction, which was unaffected by the nitric oxide synthase inhibitor l-N 5(-1-iminoethyl)ornithine (NIO; 100μmol/L). Long-term treatment (6h) with 17β-oestradiol (10 μmol/L) did not affect acetylcholine-mediated vasorelaxation in endothelium-intact aortic rings, but did attenuate PE-induced constriction. This attenuation was also observed in endotheliumdenuded preparations after 17β-oestradiol (10 μmol/L for 6h) and was far greater than the acute effect of 17β-oestradiol (10 μmol/L).3. The attenuation produced by 17β-oestradiol (10 μmol/L for 6 h) was significantly inhibited by concomitant treatment with cycloheximide (1 μmol/L), suggesting that protein synthesis was involved. NIO (100 μmol/L) also attenuated the effect, which suggests that the anti-constrictor effect of 17β-oestradiol occurs through the increased production of nitric oxide (NO). 17β-Oestradiol increased NO production, as assessed by the conversion of [3H]-arginine to [3H]-citrulline in rat aorta. These effects were prevented by cycloheximide and NIO. The anti-constrictor effect of oestrogen was blocked by the oestrogen receptor antagonist ICI 182780 (100nmol/L).4. Western blotting using an antibody specific for inducible nitric oxide synthase (NOS) revealed that 17β-oestradiol (10 μmol/L for 24 h) treatment induced the formation of inducible NOS protein in the aorta, an effect blocked by cycloheximide. The results indicate that 17β-oestradiol can attenuate the vasoconstrictor effect of PE by a specific receptor-mediated process that involves induction of inducible NOS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.tb02188.x
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  • 6
    Electronic Resource
    Electronic Resource
    INHIBITION BY HYDRALAZINE OF THE CONVERSION OF DOPAMINE TO NORADRENALINE IN RAT ATRIA IN VITRO AND IN VIVO (1980)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 7 (1980), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Hydralazine (10 to 2000 μnol/1) produced a concentration-dependent inhibition of the conversion of (3H)-dopamine to (3H)-noradrenaline in rat isolated atria.2. In rats treated with hydralazine (2 mg/kg, i.p.), there was an inhibition of the conversion of (3H)-dopamine to (3H)-noradrenaline in the intact atria in vivo.3. Hydralazine treatment may result in the appearance of dopamine as a significant co-transmitter in noradrenergic nerves, and this may contribute to the antihypertensive effect of hydralazine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1980.tb00101.x
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  • 7
    Electronic Resource
    Electronic Resource
    FACILITATION OF NORADRENALINE RELEASE BY ISOPRENALINE IN RAT ISOLATED ATRIA DOES NOT INVOLVE ANGIOTENSIN II FORMATION (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 16 (1989), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Rat isolated atria were incubated with 3H-noradrenaline and the intramural sympathetic nerves were stimulated at 2 Hz for 60 s. The stimulation-induced (SI) efflux of radioactivity was used as an index of release of transmitter noradrenaline.2. Isoprenaline (0.1 μmol/L) alone did not increase noradrenaline release. Cocaine (30 μmol/L) produced a 73% increase in the stimulation-induced release of noradrenaline. In the presence of cocaine, isoprenaline enhanced noradrenaline release by 22%.3. In the presence of cocaine, both angiotensin I (0.3 μmol/L) and angiotensin II (0.3. μmol/L) produced almost two-fold enhancements in the SI release of noradrenaline.4. Captopril (5 μmol/L) blocked the facilitatory effect of angiotensin I on nor-adrenaline release but did not alter that of isoprenaline.5. Saralasin (0.1 μmol/L) reduced the facilitatory effect of angiotensin II on noradrenaline release but did not alter that of isoprenaline.6. The findings indicate that the facilitation of noradrenaline release by isoprenaline in rat atria is not mediated by local formation of angiotensin II.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1989.tb02401.x
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  • 8
    Electronic Resource
    Electronic Resource
    MODULATION OF NORADRENALINE RELEASE IN VIVO THROUGH PREJUNCTIONAL α-ADRENOCEPTORS (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 14 (1987), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY1. Extensive in vitro studies have suggested that noradrenaline release from sympathetic nerve endings is modulated by α2-adrenoceptors on the terminal varicosities, activation of which by α-adrenoceptor agonists or neuronally released noradrenaline leads to inhibition of transmitter release.2. Studies in intact animals support essentially the physiological operation of this mechanism, whereas human studies have reached mixed conclusions and more information is required.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1987.tb00996.x
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  • 9
    Electronic Resource
    Electronic Resource
    Paper chromatographic separation of noradrenaline and its major metabolites
    Amsterdam : Elsevier
    Journal of Chromatography A 139 (1977), S. 218-222 
    Details
    ISSN: 0021-9673
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0021-9673(01)84149-2
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  • 10
    Electronic Resource
    Electronic Resource
    Frequency of pseudo-Gaucher cells in diagnostic bone marrow biopsies from patients with Ph-positive chronic myeloid leukaemia (1997)
    Springer
    Virchows Archiv 430 (1997), S. 139-148 
    Details
    ISSN: 1432-2307
    Keywords: Storing histiocytes ; Pseudo-Gaucher cells ; Chronic myeloid leukaemia ; Observer disagreement ; Bone marrow biopsies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pseudo-Gaucher cells (PGC) are a characteristic finding in Ph-positive CML, and prolongation of survival was observed when PGC were detected within the bone marrow. However, the conspicuous variation in the reported frequencies indicates the necessity for analysis of their natural occurrence in the bone marrow from untreated CML patients. A total of 833 diagnostic bone marrow biopsies from patients with Ph-positive CML were examined for PGC by 7 observers. Proof of PGC was based on systematic examination of Giemsa-stained slides with and without polarization at high magnification. Birefringence within the cytoplasm turned out to be highly specific for PGC. The risk of overlooking PGC was at least 80% when the number of these storing histiocytes was 70 per slide or less, and at least 50% when the total amount per slide was ≤ 250. This high risk of failure explained the disagreement among the authors. An intensive investigation by at least two observers is mandatory if results are to be evaluated in research. Under the conditions used in this study, the natural frequency of PGC within the bone marrow from untreated patients with a Ph-positive CML is much higher than assumed to date, amounting to about 70%. On the basis of these findings, the prognostic importance of PGC in CML must be evaluated critically.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01008035
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