Clonidine inhibition of pancreatic secretion in rats: A possible central site of action

Rozé, C; Chario, Jacques; Appia, Franck; Pascaud, X.; Vaille, C

doi:10.1016/0014-2999(81)90109-6

Cited by 25 publications

(7 citation statements)

References 12 publications

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“…Isoprenaline and norepi nephrine had qualitatively identical and nearly quantitatively identical effects on pan creatic enzyme secretion in our model. Other authors have confirmed this inhibitory effect with isoprenaline in dogs [17,28] and rats [10] and with phenylephrine [20] and cloni dine [20,27] in rats. These effects were suppressed by the respective antagonists propranolol, phenoxybenzamine and yohim bine.…”

Section: Amines and Protein Secretionsupporting

confidence: 57%

“…We recently reported a detailed study of the inhibitory effects of clonidine on pan creatic secretion in rats [27], This drug inhib ited both electrolyte and enzyme outputs and probably had a central site of action. This is in contrast to the other amines studied here, which inhibited only pancreatic protein ex cretion.…”

Section: Amines and Protein Secretionmentioning

confidence: 99%

“…27] and anesthetized rats [27], With less specific ago nists such as epinephrine (P > a) and norepi nephrine (a > P). a-receptor blocking by phenoxybenzamine increased the stimulatory ef fect of these amines on the pancreas [14], Similar data were obtained in the isolated perfused canine pancreas, in which norepi nephrine after phenoxybenzamine increased pancreatic secretion [32].…”

Section: Amines and Hydroelectrolytic Secretionmentioning

confidence: 99%

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Modulation of Stimulated Pancreatic Secretion by Sympathomimetic Amines in the Rat

Chariot

Rozé²,

Tour

et al. 1983

Pharmacology

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Pancreatic secretion in anesthetized rats with acute fistulas was provoked by caerulein, acetylcholine, electrical stimulation of the vagus nerves or by 2-deoxy-D-glucose (2-DG). Venous infusions of norepinephrine, isoprenaline or dopamine inhibited the 2-DG-stimulated enzyme secretion but not that provoked by caerulein, acetylcholine or vagal electrical stimulation. Intracerebroventricular administration of norepinephrine or isoprenaline also inhibited 2-DG-stimulated enzyme secretion. It was confirmed that the amines stimulated water and electrolyte secretion by the pancreas in the order of potency isoprenaline > norepinephrine > dopamine. The results are consistent with a model whereby norepinephrine and isoprenaline exert their effect on pancreatic secretion via a central inhibition of vagal drive to the pancreas, together with a direct stimulating effect on water and electrolyte secretion at the level of pancreatic cells.

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Section: Amines and Protein Secretionsupporting

confidence: 57%

Section: Amines and Protein Secretionmentioning

confidence: 99%

Section: Amines and Hydroelectrolytic Secretionmentioning

confidence: 99%

See 1 more Smart Citation

Modulation of Stimulated Pancreatic Secretion by Sympathomimetic Amines in the Rat

Chariot

Rozé²,

Tour

et al. 1983

Pharmacology

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“…dry mouth [130,131]. In addition, we demonstrated that clonidine relieves all types of pancreatic pain, which should be attributed to the reduction of the flow of pancreatic juice [6-8, 15-17, 20-22, 45, 51, 87, 89, 90, 95-97, 107, 109, 121, 131-147].…”

Section: Pancreatitismentioning

confidence: 94%

Central Nervous System Plus Autonomic Nervous System Disorders Responsible for Gastrointestinal and Pancreatobiliary Diseases

Lechín

Dijs

2008

Dig Dis Sci

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Clinical digestive disorders depend on the nonadequate coupling of functioning of the gastrointestinal tract with that of its affluent systems, namely, the pancreatic exocrine and the hepato-biliary secretions. The secretion of gastrointestinal hormones is monitored by the peripheral autonomic nervous system. However, the latter is regulated by the central nervous system (CNS) circuitry localized at the medullary pontine segment of the CNS. In turn, both parasympathetic and adrenergic medullary circuitries are regulated by the pontine A5 noradrenergic (NA) and the dorsal raphe serotonergic nuclei, respectively. DR-5HT is positively correlated with the C1-Ad medullary nuclei (responsible for adrenal gland secretion), whereas the MR-5HT nucleus is positively correlated with the A5-NA pontomedullary nucleus. The latter is responsible for neural sympathetic activity (sympathetic nerves). Both types of sympathetic activities maintain an alternation with the peripheral parasympathetic branch, which is positively correlated with the enterochromaffin cells that secrete serotonin. Serotonin displays hormonal antagonism to the circulating catecholamines.

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“…Thus, in high IT-low NE plasma level subjects, it is difficult to attribute the pro nounced biochemical, physiological, and endocrinological changes induced by clonidine to the small decrease in al ready low plasma NE level registered in the present study. On the other hand, evidence suggests that cardiovascular [12], pancreatic [44], and gastrointestinal [23,42,43] effects are triggered by the drug through central mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Effects of Clonidine on Blood Pressure, Noradrenaline, Cortisol, Growth Hormone, and Prolactin Plasma Levels in High and Low Intestinal Tone Subjects

Lechín¹,

Dijs²,

Jakubowicz³

et al. 1985

Neuroendocrinology

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Systolic blood pressure (SBP), diastolic blood pressure (DBP), norepinephrine (NE), cortisol (CRT), growth hormone (GH), and prolactin (PRL) plasma levels were investigated in 46 normal subjects, 28 high intestinal tone (high IT) and 18 low intestinal tone (low IT), before and after the administration of a single intramuscular dose of clonidine (2.5 µg/kg). High IT subjects had lower mean values of DBP than low IT subjects, and basal NE was significantly greater in low IT than in high IT subjects. A negative correlation between NE and IT values was found for the high IT, but not for the low IT group, during the preclonidine periods. The drug reduced SBP in high IT, whereas it reduced SBP plus DBP and NE in low IT subjects. Clonidine induced significant reductions of CRT and increases of GH in both groups; furthermore, a slight but significant reduction of PRL was registered in high IT group. The drug also induced increase of distal colon tone in high IT subjects and suppressed phasic activity (waves) in low IT subjects. While a significant positive correlation was found between NE and DBP in low IT subjects during postclonidine periods, no correlation was found between the two parameters in high IT subjects. Other significant positive (+) and negative (–) correlations during postclonidine periods were: CRT/GH (–), CRT/PRL (+), and GH/PRL (–) in high IT subjects; NE/CRT (+), NE/GH (–), CRT/GH (–), CRT/DBP (+), and GH/DBP (-) in low IT subjects. Finally, significant negative correlation was found between NE and distal colon tone during postclonidine periods in high IT subjects. Our results suggest that there is a sympathetic (NE) hypoactivity in high IT subjects and a sympathetic (NE) hyperactivity in low IT subjects. Postsynaptic and presynaptic pharmacological mechanisms are postulated in order to explain these two different patterns of responses to the challenge of clonidine.

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Clonidine inhibition of pancreatic secretion in rats: A possible central site of action

Cited by 25 publications

References 12 publications

Modulation of Stimulated Pancreatic Secretion by Sympathomimetic Amines in the Rat

Modulation of Stimulated Pancreatic Secretion by Sympathomimetic Amines in the Rat

Central Nervous System Plus Autonomic Nervous System Disorders Responsible for Gastrointestinal and Pancreatobiliary Diseases

Effects of Clonidine on Blood Pressure, Noradrenaline, Cortisol, Growth Hormone, and Prolactin Plasma Levels in High and Low Intestinal Tone Subjects

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