The release of catecholamines from the adrenal medulla and its modulation by α2-adrenoceptors in the anaesthetized dog

1987 ◽  
Vol 65 (4) ◽  
pp. 550-557 ◽  
Author(s):  
Sylvain Foucart ◽  
Réginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Medulla ◽  
Plasma Concentrations ◽  
Splanchnic Nerve ◽  
Feedback Mechanism ◽  
Adrenal Vein ◽  
Low Frequencies ◽  
Negative Feedback Mechanism ◽  
Frequency Of Stimulation ◽  
Stimulation Of

The adrenal nerve of anaesthetized and vagotomized dogs was electrically stimulated (10 V pulses of 2 ms duration for 10 min) at frequencies of 1, 3, 10, and 25 Hz. There was a correlation between the frequency of stimulation and the plasma concentrations of epinephrine, norepinephrine, and dopamine in the adrenal vein, mainly after the 1st min of stimulation and the maximal concentration was reached sooner with higher frequencies of stimulation. Moreover, the relative percentage of catecholamines released in response to the electrical stimulation was not changed by the frequency of stimulation. To test the hypothesis that a local negative feedback mechanism mediated by α2-adrenoceptors exists in the adrenal medulla, the effects of the systemic administration of clonidine (α2-agonist) and yohimbine (α2-antagonist) on the concentrations of catecholamines in the adrenal vein were evaluated during the electrical stimulation of the adrenal nerve (5 V pulses of 2 ms duration for 3 min) at 3 Hz. Moreover, the effects of the systemic injections of more specific α2-agonist and antagonist (oxymetazoline and idazoxan) were tested on the release of catecholamines in the adrenal vein in response to electrical stimulation of the splanchnic nerve at 1 and 3 Hz frequencies. The injection of 0.5 mg/kg of yohimbine caused a significant increase in the concentrations of epinephrine and norepinephrine in the adrenal vein induced by the electrical stimulation of the adrenal nerve and the injection of 15 μg/kg of clonidine had no effects. In the second series of experiments, the injection of 2 μg/kg of oxymetazoline caused a significant decrease in the release of epinephrine and norepinephrine at 1 Hz, but similarly to clonidine, there were no changes at 3 Hz. In contrast, the release of epinephrine and dopamine in response to electrical stimulation of the splanchnic nerve was increased at 3 Hz after the injection of idazoxan, but not at 1 Hz. It is concluded that the adrenal medulla catecholamines secretion appears to be partly modulated by a presynaptic inhibitory mechanism that involves α2-adrenoceptors. The observation that agonists appear to be more efficient at low frequencies of stimulation while antagonists appear to be more efficient at higher frequencies could be explained by the possibility that adrenal medullary α2-receptors would be saturated at higher frequencies of stimulation.

scholarly journals Submicroscopic Changes of the Nerve Endings in the Adrenal Medulla after Stimulation of the Splanchnic Nerve

1957 ◽  
Vol 3 (4) ◽  
pp. 611-614 ◽  
Author(s):  
Eduardo De Robertis ◽  
Alberto Vaz Ferreira
Keyword(s):  
Electrical Stimulation ◽  
Electron Microscope ◽  
Adrenal Medulla ◽  
Synaptic Vesicles ◽  
Splanchnic Nerve ◽  
The Other ◽  
Nerve Endings ◽  
The Mean ◽  
Increased Activity ◽  
Stimulation Of

The nerve endings of the adrenal medulla of the rabbit were studied under the electron microscope in the normal condition and after prolonged electrical stimulation of the splanchnic nerve. With a stimulus of 100 pulses per second for 10 minutes, there is an increase in the number of synaptic vesicles in the nerve ending. The mean number is of 82.6 vesicles per square micron in the normal and of 132.7 per square micron in the stimulated glands. With a stimulus of 400 pulses per second for 10 minutes, there is a considerable depletion of synaptic vesicles and other changes occur in the nerve endings. The mean number of vesicles is of 29.2 per square micron. These results are interpreted as indicative of an increased activity of the ending in one case, and as a diminished activity and fatigue of the synaptic junction in the other.

In vivo interactions between prejunctional α2- and β2-adrenoceptors at the level of the adrenal medulla

1988 ◽  
Vol 66 (10) ◽  
pp. 1340-1343 ◽  
Author(s):  
Sylvain Foucart ◽  
Jacques de Champlain ◽  
Réginald Nadeau
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Medulla ◽  
Intravenous Injection ◽  
Splanchnic Nerve ◽  
Inhibitory Effect ◽  
Significant Rise ◽  
Catecholamine Release ◽  
Control Stimulation ◽  
Stimulation Of

The combined effect of a β2-antagonist and an α2-agonist on the release of adrenal catecholamines was studied in the anaesthetized and vagotomized dog. The electrical stimulation of the splanchnic nerve (5-V pulses of 2 ms duration for 3 min at a frequency of 3 Hz) produced a significant rise in adrenal catecholamine release in the adrenal vein. Intravenous injection of a β2-antagonist significantly reduced this response and a subsequent injection of an α2-agonist further reduced the release of catecholamines. However, if the α2-agonist is injected first, the release is not different compared with the control stimulation, and the subsequent injection of the β2-antagonist also did not modify the release in response to electrical stimulation. These results suggest that the blockade of presynaptic β2-receptors reduces the release of adrenal catecholamines without interfering with the activation of the α2-adrenoceptors. In contrast, the pretreatment with the α2-agonist, which does not modify the release of catecholamine at 3 Hz, seems to interfere with the inhibitory effect of the β2-antagonist.

Adrenal versus nonadrenal sympathetic preganglionic neurones in the lower thoracic intermediolateral nucleus of the cat: physiological properties

1990 ◽  
Vol 68 (11) ◽  
pp. 1447-1456 ◽  
Author(s):  
S. B. Backman ◽  
H. Sequeira-Martinho ◽  
J. L. Henry
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Medulla ◽  
Splanchnic Nerve ◽  
Physiological Properties ◽  
Preganglionic Neurone ◽  
Spinal Segments ◽  
The Mean ◽  
Greater Splanchnic Nerve ◽  
Intermediolateral Nucleus ◽  
Stimulation Of

Adrenal and nonadrenal sympathetic preganglionic neurones (SPNs) in the intermediolateral nucleus of spinal segments T8–T10 in the cat were compared according to a number of physiological properties. An SPN was classified as "adrenal" (n = 37) if it could be antidromically activated by electrical stimulation of the adrenal medulla. An SPN that could not be activated from the adrenal medulla yet could be antidromically activated by electrical stimulation of the greater splanchnic nerve was classified as "nonadrenal" (n = 123). Approximately 50% of adrenal SPNs (17 out of 37) were activated antidromically by stimulation of both the greater splanchnic nerve and adrenal medulla, suggesting that these neurones projected to the adrenal medulla via the greater splanchnic nerve, with the other adrenal SPNs taking a different route. The mean conduction velocities of adrenal (6.7 ± 1.8 (SD) m/s) and nonadrenal (6.7 ± 1.5 m/s) sympathetic preganglionic axons were similar. Over 80% of adrenal (31 out of 37) and nonadrenal (104 out of 116) SPNs were spontaneously active. The two types of neurone were indistinguishable in terms of the rates and patterns of discharge. Adrenal SPNs discharged with a mean rate of 1.4 ± 1.1 spikes/s, and nonadrenal SPNs discharged with a mean rate of 1.8 ± 1.4 spikes/s. With both types of SPN, the pattern of spontaneous activity was either irregular or phasic. With the latter pattern, periodic bursts of discharge were at the same frequency as oscillations in arterial pressure, frequency of ventilation, or phrenic nerve discharge. These data suggest that adrenal and nonadrenal sympathetic preganglionic neurones in the intermediolateral nucleus in caudal thoracic segments share a number of common physiological properties.Key words: adrenal, sympathetic preganglionic neurone, spinal cord, lateral horn.

Effect of changes in myocardial epinephrine stores on plasma norepinephrine gradient across the dog heart

1994 ◽  
Vol 266 (6) ◽  
pp. H2404-H2409 ◽  
Author(s):  
F. Peronnet ◽  
G. Boudreau ◽  
J. de Champlain ◽  
R. Nadeau
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Medulla ◽  
Pulse Width ◽  
Stellate Ganglion ◽  
Plasma Norepinephrine ◽  
Direct Support ◽  
Left Stellate Ganglion ◽  
Ici 118,551 ◽  
Beta 2 ◽  
Stimulation Of

Plasma norepinephrine (NE) concentration ([NE]) gradient across the heart was measured under electrical stimulation of the left stellate ganglion (LSG; 4 Hz, 4 V, 2 ms pulse width, 1 min) in control (Ctrl) and in adrenalectomized (Adrx) dogs, without and with a 10-min epinephrine (Epi) infusion (92 ng.kg-1.min-1), which partly restored myocardial Epi stores in Adrx dogs (2.9 +/- 0.7 ng/g vs. 6.4 +/- 0.7 ng/g in Ctrl dogs) and slightly increased tissue Epi stores in Ctrl dogs (10.5 +/- 1.3 pg/g). Compared with Ctrl dogs (1,069 +/- 172 pg/ml), the [NE] gradient across the heart under stimulation of the LSG was not modified 1 wk after bilateral adrenalectomy (1,190 +/- 122 pg/ml) or after Epi infusion in Ctrl (1,134 +/- 276 pg/ml) and Adrx (1,259 +/- 279 pg/ml) dogs. The beta 2-antagonist ICI-118,551 significantly reduced the stimulation-induced [NE] gradient across the heart in Ctrl dogs (621 +/- 190 and 603 +/- 86 pg/ml without and with a 10-min Epi infusion, respectively) but not in Adrx dogs deprived of tissue Epi (1,345 +/- 345 pg/ml). Partial repletion of myocardial Epi stores in Adrx dogs restored the effect of ICI-118,551 on the stimulation-induced [NE] gradient (776 +/- 121 pg/ml). These results provide direct support of the hypothesis that tissue Epi, which originates from the adrenal medulla and which is released locally along with NE, is the endogenous agonist for presynaptic beta 2-receptors and potentiates NE release.

scholarly journals Pancreatic and extrapancreatic galanin release during sympathetic neural activation

1990 ◽  
Vol 258 (3) ◽  
pp. E436-E444 ◽  
Author(s):  
B. E. Dunning ◽  
P. J. Havel ◽  
R. C. Veith ◽  
G. J. Taborsky
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Sympathetic Nerves ◽  
Neural Activation ◽  
Anesthetized Dogs ◽  
Basal Insulin Secretion ◽  
Peripheral Arterial ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

To address the hypothesis that the neutropeptide, galanin, functions as a sympathetic neurotransmitter in the endocrine pancreas, we sought to determine if galanin is released from pancreatic sympathetic nerves during their direct electrical stimulation in halothane-anesthetized dogs. During bilateral thoracic splanchnic nerve stimulation (BTSNS), both peripheral arterial and pancreatic venous levels of galanin-like immunoreactivity (GLIR) increased (delta at 10 min = +92 +/- 31 and +88 +/- 25 fmol/ml, respectively). Systemic infusions of synthetic galanin demonstrated that 1) the increment of arterial GLIR observed during BTSNS was sufficient to modestly restrain basal insulin secretion and 2) only 25% of any given increment of arterial GLIR appears in the pancreatic vein, suggesting that the pancreas extracts galanin, as it does other neurotransmitters. By use of 75% for pancreatic extraction of circulating galanin, it was calculated that pancreatic galanin spillover (output) increased by 410 +/- 110 fmol/min during BTSNS. To reinforce the conclusion that pancreatic sympathetic nerves release galanin, GLIR spillover was next measured during direct local stimulation of the pancreatic sympathetic input produced by electrical stimulation of the mixed autonomic pancreatic nerves (MPNS) in the presence of the ganglionic blocker, hexamethonium. During this local pancreatic sympathetic nerve stimulation, arterial GLIR remained unchanged, but pancreatic venous GLIR increased by 123 +/- 34 fmol/ml. Thus pancreatic GLIR spillover increased by 420 +/- 110 fmol/min during MPNS in the presence of hexamethonium. We conclude that galanin is released from both pancreatic and extrapancreatic sources during sympathetic neural activation in dogs.

In vivo modulation by α2-adrenoceptors of adrenal catecholamine release in the anaesthetized dog

1988 ◽  
Vol 66 (3) ◽  
pp. 380-384 ◽  
Author(s):  
Sylvain Foucart ◽  
Jacques de Champlain ◽  
Reginald Nadeau
Keyword(s):  
Electrical Stimulation ◽  
Splanchnic Nerve ◽  
Catecholamine Release ◽  
Agonist Stimulation ◽  
Control Stimulation ◽  
Anaesthetized Dog ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

In this study, the reversal of the potentiating effect of idazoxan, a selective α2-antagonist, on adrenal catecholamine release elicited by splanchnic nerve stimulation in anaesthetized and vagotomized dogs, was investigated with the use of oxymetazoline, a selective α2-agonist. Stimulation of the left splanchnic nerve (5.0-V pulses of 2 ms duration for 3 min at a frequency of 2 Hz) was applied before and 20 min after the i. v. injection of each drug. Blood samples were collected in the adrenal vein before and at the end of each stimulation. The results show that the release of catecholamines induced by electrical stimulation was potentiated by 50% after idazoxan injection (0.1 mg/kg). This enhanced response was significantly antagonized by the subsequent injection of oxymetazoline (2 μg/kg). The α2-modulating effect appears to be related to the amount of catecholamines released during the stimulation, since by subgrouping of the data on the basis of the degree of potentiation by idazoxan, it was observed that this drug was more efficient when catecholamine release was higher during control stimulation. In contrast, the reversing effect of oxymetazoline was found to be more pronounced when catecholamine release was lower. These results thus suggest that the sensitivity of the α2-adrenoceptor mechanism may depend upon the in situ concentration of adrenal catecholamine release during electrical stimulation and that the potentiating effect of α2-blockade can be reversed by activation of those receptors by a selective α2-agonist.

Effectiveness of Middle Ear Electrical Stimulation for Activating Central Auditory Pathways

1982 ◽  
Vol 91 (3) ◽  
pp. 285-291 ◽  
Author(s):  
Ben M. Clopton ◽  
Martha M. Bosma
Keyword(s):  
Electrical Stimulation ◽  
Guinea Pig ◽  
Middle Ear ◽  
Spiral Ganglion ◽  
Auditory Pathways ◽  
Low Frequencies ◽  
Central Auditory Pathways ◽  
Stimulation Of

Electrical stimulation of afferent auditory elements through electrodes placed in the middle ear was investigated in acute guinea pig preparations. Thresholds for auditory activation were current-dependent for low frequencies (<1 kHz) and charge-dependent at higher frequencies. Threshold currents were 3–5 times those for intracochlear stimulation. Mechanisms of activation were examined with removal of cochlear fluids and injection of neomycin, Xylocaine, saline, and artificial perilymph with different calcium concentrations. Neurons of the spiral ganglion are indicated as mediators of this stimulation.

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