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  • 1
    Electronic Resource
    Electronic Resource
    Cardiovascular effects of agmatine, a “clonidine-displacing substance”, in conscious rabbits (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 268-273 
    Details
    ISSN: 1432-1912
    Keywords: Agmatine ; Yohimbine ; Clonidine-displacing substance ; α2-Adrenoceptors Imidazoline receptors ; Blood pressure ; Sympathetic nerve activity ; Cardiovascular regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Agmatine has been identified as a “clonidine-displacing substance” in extracts from bovine brain. We studied its effect on cardiovascular regulation and the role played in this effect by α2-adrenoceptors. In conscious rabbits, agmatine 10 μg kg−1 injected intracisternally (i.e.) caused no change, whereas agmatine 30, 100 and 300 μg kg−1 i.e. increased renal sympathetic nerve firing, the plasma concentration of noradrenaline and adrenaline and arterial blood pressure. Heart rate tended to be decreased. Yohimbine 1.5 μg kg−1 i.e. caused no change, whereas yohimbine 5, 15 and 50 μg kg−1 increased renal sympathetic nerve activity, the plasma concentration of noradrenaline and adrenaline, blood pressure and heart rate. In rabbit brain cortex slices preincubated with [3H]-noradrenaline, agmatine 1 to 100 μM did not modify the electrically evoked overflow of tritium (either 4 pulses at 100 Hz or 36 pulses at 3 Hz). The evoked overflow was reduced by 5-bromo-6-(2-imidazolin-2-ylamino)quinoxaline (UK 14304) 0.03 to 30 nM (4 pulses at 100 Hz), and this inhibition was not affected by agmatine 10 and 100 μM. Agmatine did not change the basal efflux of tritium. The results show that agmatine, like yohimbine, causes central sympathoexcitation when given i.e., but agmatine differs from yohimbine in that it does not increase heart rate. Agmatine acts neither as an agonist nor as an antagonist at the α2-autoreceptors in rabbit brain cortex. α2-Adrenoceptors, therefore, are probably not involved in its cardiovascular effects. An action at imidazoline receptors in the medulla oblongata or some other hitherto unknown mechanism may be responsible for the sympathoexcitation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233246
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  • 2
    Electronic Resource
    Electronic Resource
    Desipramine inhibits sympathetic nerve activity in the rabbit (1990)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 342 (1990), S. 469-476 
    Details
    ISSN: 1432-1912
    Keywords: Anaesthetized rabbit ; Noradrenaline spillover rate ; Sympathoinhibition ; Sympathetic nerve activity ; Uptake inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of the study was to determine the sites of action of intravenously administered desipramine on the sympathetic nervous system in anaesthetized rabbits (alfadolone + alfaxalone). Renal postganglionic sympathetic nerve activity was measured in order to determine central nervous and ganglionic effects. The clearance of noradrenaline from the plasma was determined with an isotope tracer method. From the noradrenaline clearance and the plasma concentration of noradrenaline the noradrenaline spillover rate was calculated. These parameters as well as blood pressure and heart rate were measured before (basal values) and at the end of 20-min infusions of sodium nitroprusside, which was given in order to modulate efferent sympathetic nerve activity through the baroreceptors. Desipramine 0.5 mg kg-1 + 0.05 mg kg−1 h−1 (bolus injection followed by infusion) and 2 mg kg−1 + 0.2 mg kg−1 h−1 dose-dependently inhibited basal sympathetic nerve activity and the noradrenaline clearance. Desipramine had no effect on basal blood pressure, noradrenaline spillover rate or heart rate. Nitroprusside produced hypotension and simultaneously increased sympathetic nerve activity, noradrenaline spillover rate and heart rate; the clearance of noradrenaline was reduced with decreasing blood pressure. The relationship between sympathetic nerve activity and blood pressure was shifted by desipramine in a manner indicating central sympathoinhibition. Desipramine had no effect on the relationship of the noradrenaline spillover rate to blood pressure, whereas it shifted the heart rate-blood pressure relationship in a manner indicating an enhancement of reflex cardioacceleration. In a separate series of experiments, desipramine also inhibited sympathetic nerve activity in baroreceptor-denervated animals. The results show that desipramine centrally inhibits sympathetic outflow in the rabbit. Simultaneously, it enhances the noradrenaline spillover per action potential peripherally. In our study, the two effects compensated for each other, so that desipramine had no major effect on the relationship between noradrenaline spillover and blood pressure. In the heart, the peripheral effect of desipramine outweighed the central sympathoinhibition, hence the reflex cardioacceleration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169466
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  • 3
    Electronic Resource
    Electronic Resource
    Inhibition of uptake1 by (+)-oxaprotiline reveals a differential central regulation of noradrenaline and adrenaline release (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 249-257 
    Details
    ISSN: 1432-1912
    Keywords: Antidepressant drugs ; (+)-Oxaprotiline ; Prazosin ; Uptake ; α1-Adrenoceptors ; Noradrenaline release ; Adrenaline release ; Sympathetic outflow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Inhibition of uptake, in the central nervous system leads to a decrease of sympathetic outflow to many tissues; central a2-adrenoceptors are involved in this decrease. The aim of the present study was to compare the effects of the selective uptake, inhibitor (+)-oxaprotiline on the plasma kinetics of noradrenaline and adrenaline in anaesthetized and in conscious rabbits. [3H]Noradrenaline and [3H]adrenaline were infused iv. The arterial plasma concentrations of endogenous and radiolabelled noradrenaline and adrenaline were measured, and the clearance from and spillover into the plasma of noradrenaline and adrenaline were calculated. Results obtained in conscious and anaesthetized rabbits were similar. (+)-Oxaprotiline 0.2, 0.6 and 1.8 mg kg−1 iv. dose-dependently reduced the clearance of [3H]noradrenaline from the plasma. The clearance of [3H]adrenaline was reduced less. The spillover of endogenous noradrenaline was decreased by up to 35%. In contrast, the spillover of adrenaline tended to be enhanced. Prazosin 0.1 and 1 mg kg−1 was injected iv. in a second part of each experiment. It lowered the blood pressure and caused a marked increase in noradrenaline spillover but no increase or even a decrease in adrenaline spillover. The results are compatible with the following hypothesis. The sympathetic outflow from the central nervous system is subject to a twofold a-adrenoceptor-mediated modulation: α-adrenoceptor-mediated inhibition and α1-adrenoceptor-mediated excitation. In the control of the sympathetic outflow to many extra-adrenal tissues, the α2-adrenergic inhibition prevails. Uptake1 inhibitors depress sympathetic outflow to such tissues by enhancing the α2-adrenergic inhibition. In the regulation of the sympathetic outflow to the adrenal medulla, in contrast, α2-adrenergic inhibition and α1-adrenergic excitation have a similar impact. Uptake, inhibitors, hence, cause little change in adrenaline release: the two opposing influences cancel out. Prazosin produces an increase in noradrenaline but not adrenaline release because the loss of the central α1 sympathoexcitation attenuates at best slightly the baroreflex to most extra-adrenal tissues but dampens markedly the baroreflex to the adrenal medulla.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169152
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  • 4
    Electronic Resource
    Electronic Resource
    Peripheral presynaptic and central effects of clonidine, yohimbine and rauwolscine on the sympathetic nervous system in rabbits (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 648-657 
    Details
    ISSN: 1432-1912
    Keywords: Anaesthetized rabbit ; Blood pressure ; Plasma noradrenaline concentration ; Presynaptic α2-autoreceptors ; Sympathetic nerve activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The function of presynaptic α2-autoreceptors at postganglionic sympathetic neurones under conditions of normal, ongoing sympathetic impulse traffic was studied in anaesthetized rabbits (alfadolone + alfaxalone). Clonidine was used as an α2-adrenoceptor agonist, and yohimbine and rauwolscine were used as antagonists. Mean arterial pressure, postganglionic renal sympathetic firing rate, arterial plasma noradrenaline concentration and heart rate were measured before (basal values) and at the end of 3-min infusions of sodium nitroprusside and phenylephrine, which were given to modulate efferent activity in the sympathetic nervous system through the baroreflex. The nitroprusside- and phenylephrine-induced changes of mean arterial pressure produced the expected changes in sympathetic nerve activity, plasma noradrenaline and heart rate. Clonidine (5 µg kg−1 + 0.5 µg kg−1 min−1) reduced the basal mean arterial pressure, sympathetic nerve activity and heart rate. It also reduced the nitroprusside-induced increase in the plasma noradrenaline level without changing the nitroprusside-induced increase in sympathetic firing. These results, as well as the mean arterial pressure-sympathetic nerve activity and the sympathetic nerve activity-plasma noradrenaline function curves indicate that clonidine inhibited both sympathetic tone centrally and the average release of noradrenaline per action potential peripherally. Yohimbine (1 mg kg−1 + 0.1 mg kg−1 h−1) and rauwolscine (0.5 mg kg−1 + 0.1 mg kg−1 h−1) increased the basal plasma noradrenaline level without any increase of renal sympathetic nerve activity. They also enhanced the nitroprusside-induced increase in plasma noradrenaline without any enhancement of the nitroprusside-induced increase in sympathetic firing. The hypotensive response to nitroprusside was attenuated, whereas the heart rate response was augmented. These results, as well as the mean arterial pressure-sympathetic nerve activity and the sympathetic nerve activity-plasma noradrenaline function curves indicate that the main effect of yohimbine and rauwolscine was to increase the average release of noradrenaline per action potential. The simultaneous measurement of postganglionic sympathetic nerve activity and the arterial plasma noradrenaline concentration proved suitable to differentiate central (or ganglionic; this distinction was not possible) effects of α2-adrenoceptor ligands from peripheral presynaptic effects. The results show that endogenous presynaptic, α2-adrenergic autoinhibition of noradrenaline release from postganglionic sympathetic neurones operates physiologically in anaesthetized rabbits with ongoing, uninterrupted sympathetic nerve activity. The results also indicate that blockade of α2-autoreceptors enhances the sympathetic reflex compensatory response to a hypotensive stimulus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00717740
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    Paper (German National Licenses)
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