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

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.

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y88-064 ◽

1988 ◽

Vol 66 (3) ◽

pp. 380-384 ◽

Cited By ~ 2

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.

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-093 ◽

1987 ◽

Vol 65 (4) ◽

pp. 550-557 ◽

Cited By ~ 12

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.

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

The Journal of Cell Biology ◽

10.1083/jcb.3.4.611 ◽

1957 ◽

Vol 3 (4) ◽

pp. 611-614 ◽

Cited By ~ 73

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.

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y90-219 ◽

1990 ◽

Vol 68 (11) ◽

pp. 1447-1456 ◽

Cited By ~ 7

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.

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Greater splanchnic excitation of primate T1-T5 spinothalamic neurons

Journal of Neurophysiology ◽

10.1152/jn.1984.51.3.592 ◽

1984 ◽

Vol 51 (3) ◽

pp. 592-603 ◽

Cited By ~ 37

Author(s):

W. S. Ammons ◽

R. W. Blair ◽

R. D. Foreman

Keyword(s):

Electrical Stimulation ◽

Cell Activation ◽

Receptive Fields ◽

Splanchnic Nerve ◽

Inhibitory Effect ◽

Sympathetic Stimulation ◽

Bilateral Vagotomy ◽

Somatic Receptive Fields ◽

Greater Splanchnic Nerve ◽

Stimulation Of

Effects of electrical stimulation of the left greater splanchnic nerve (SPL) on T1-T5 spinothalamic (STT) neurons were determined. Eighty-five STT neurons were studied in 36 anesthetized monkeys (Macaca fascicularis). All neurons were excited by manipulation of their somatic receptive fields and by electrical stimulation of cardiopulmonary (CP) sympathetic afferent fibers. SPL stimulation excited 63 (74%) STT neurons. There was an increasing percentage of cells with SPL input at more caudal segments and in deeper laminae. Both SPL and CP sympathetic stimulation elicited early or both early and late responses. Latencies to cell activation were usually shorter for CP sympathetic stimulation than for SPL stimulation (5.4 +/- 0.8 versus 11.3 +/- 2.0 ms for early responses and 44.2 +/- 4.2 versus 111.0 +/- 6.6 ms for late responses). The maximum number of spikes per SPL or CP sympathetic stimulus was determined. In the T2 and T3 segments, early responses to CP sympathetic stimulation were significantly greater. However, at more caudal segments, responses to CP sympathetic input decreased while responses to SPL input increased until at T4 there was no difference in the two responses. In T5, responses to SPL input were greater. No differences in the magnitudes of late responses were observed in any of the segments. The response of six cells to SPL stimulation was inhibited by a train of conditioning stimuli applied to the left thoracic vagus nerve. Maximum inhibition occurred at a CT interval of 50 ms and test responses were significantly reduced at CT intervals as great as 200 ms. Bilateral vagotomy eliminated the inhibitory effect. Cutting the left sympathetic chain between the T5 and T6 rami communicantes eliminated 27% of the response to SPL stimulation. More caudal cuts reduced the response further until 71% of the response was abolished by a cut between T8 and T9. Lesions in the dorsolateral column of the spinal cord had little effect on the responses, while lesions of the lateral and ventrolateral columns reduced or abolished the responses. We conclude that SPL stimulation excites T1-T5 STT neurons by way of extraspinal and intraspinal pathways. SPL information is integrated with information from a variety of other visceral and somatic sources. SPL input to cells with somatic fields in the chest region may explain the clinical phenomenon of chest pain associated with abdominal disorders.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.6.h2404 ◽

1994 ◽

Vol 266 (6) ◽

pp. H2404-H2409 ◽

Cited By ~ 2

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.

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Somatostatin modulates cholinergic neurotransmission in canine antral muscle

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1988.254.2.g201 ◽

1988 ◽

Vol 254 (2) ◽

pp. G201-G209 ◽

Cited By ~ 1

Author(s):

C. B. Koelbel ◽

G. van Deventer ◽

S. Khawaja ◽

M. Mogard ◽

J. H. Walsh ◽

...

Keyword(s):

Electrical Stimulation ◽

Substance P ◽

Prostaglandin E2 ◽

Positive Inotropic Effect ◽

Mechanical Response ◽

Inhibitory Effect ◽

Inotropic Effect ◽

Inotropic Response ◽

Cholinergic Neurotransmission

Somatostatin has been shown to inhibit antral motility in vivo. To examine the effect of somatostatin on cholinergic neurotransmission in the canine antrum, we studied the mechanical response of and the release of [3H]acetylcholine from canine longitudinal antral muscle in response to substance P, gastrin 17, and electrical stimulation. In unstimulated tissues, somatostatin had a positive inotropic effect on spontaneous phasic contractions. In tissues stimulated with substance P and gastrin 17, but not with electrical stimulation, somatostatin inhibited the phasic inotropic response dose dependently. This inhibitory effect was abolished by indomethacin. Somatostatin stimulated the release of prostaglandin E2 radioimmunoreactivity, and prostaglandin E2 inhibited the release of [3H]acetylcholine induced by substance P and electrical stimulation. Somatostatin increased the release of [3H]acetylcholine from unstimulated tissues by a tetrodotoxin-sensitive mechanism but inhibited the release induced by substance P and electrical stimulation. These results suggest that somatostatin has a dual modulatory effect on cholinergic neurotransmission in canine longitudinal antral muscle. This effect is excitatory in unstimulated tissues and inhibitory in stimulated tissues. The inhibitory effect is partially mediated by prostaglandins.

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Cross-talk along gastrointestinal tract during electrical stimulation: effects and mechanisms of gastric/colonic stimulation on rectal tone in dogs

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00554.2004 ◽

2005 ◽

Vol 288 (6) ◽

pp. G1195-G1198 ◽

Cited By ~ 15

Author(s):

Shi Liu ◽

Lijie Wang ◽

J. D. Z. Chen

Keyword(s):

Electrical Stimulation ◽

Inhibitory Effect ◽

Adrenergic Blockade ◽

Rectal Compliance ◽

Rectal Tone ◽

Before And After ◽

Sensory Functions ◽

Sympathetic Pathway ◽

Colonic Electrical Stimulation ◽

Stimulation Of

Gastric electrical stimulation (GES) has been shown to alter motor and sensory functions of the stomach. However, its effects on other organs of the gut have rarely been investigated. The study was performed in 12 dogs implanted with two pairs of electrodes, one on the serosa of the stomach and the other on the colon. The study was composed of two experiments. Experiment 1 was designed to study the effects of GES on rectal tone and compliance in nine dogs compared with colonic electrical stimulation (CES). Rectal tone and compliance were assessed before and after GES or CES. Experiment 2 was performed to study the involvement of sympathetic pathway in 8 of the 12 dogs. The rectal tone was recorded for 30–40 min at baseline and 20 min after intravenous guanethidine. GES or CES was given for 20 min 20 min after the initiation of the infusion. It was found that both GES and CES reduced rectal tone with comparable potency. Rectal compliance was altered neither with GES, nor with CES. The inhibitory effect of GES but not CES on rectal tone was abolished by an adrenergic blockade, guanethidine. GES inhibited rectal tone with a comparable potency with CES but did not alter rectal compliance. The inhibitory effect of GES on rectal tone is mediated by the sympathetic pathway. It should be noted that electrical stimulation of one organ of the gut may have a beneficial or adverse effect on another organ of the gut.

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