Central and peripheral inhibition of exocrine pancreatic secretion by alpha-2 adrenergic agonists in the rat

Cheriot, J.; Appia, F.; Tacca, M. Del; Tsocas, Annick; Rozé, C

doi:10.1016/s0031-6989(88)80118-8

Cited by 12 publications

(4 citation statements)

References 7 publications

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“…This finding suggests that there was disruption not only of stimulatory fibers but of sympathetic fibers that maintain tonic constriction of pancreatic vessels. 122,123 Norepinephrine is believed to be the primary transmitter released by intrapancreatic adrenergic nerves. Various reports describe norepinephrine stimulating, inhibiting, or having no effect on pancreatic secretion.…”

Section: Adrenergic Nervesmentioning

confidence: 99%

Regulation of Pancreatic Secretion

Liddle¹

2012

Physiology of the Gastrointestinal Tract

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Section: Adrenergic Nervesmentioning

confidence: 99%

Regulation of Pancreatic Secretion

Liddle¹

2012

Physiology of the Gastrointestinal Tract

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“…The degree of inhibition by ST91 was significant but still less than that of clonidine, an observation which suggests that both peripheral and central alpha 2 -adrenoceptor activation inhibits icilin-induced shaking. Support for this interpretation is provided by in vivo studies in rats which demonstrated that the potency of ST91 is about ten times less than that of clonidine following systemic injection, whereas ST91 displays the same degree of potency as clonidine after injections into the cerebral ventricles (Chariot et al, 1988; Taylor et al, 1988; Eshel et al, 1990). Furthermore, ST91, when administered by the same route and within the same dose range (0.075 – 0.15 mg/kg) as in our study, did not alter the extent of shaking precipitated by naloxone in morphine-dependent rats (Taylor et al, 1988).…”

Section: Discussionmentioning

confidence: 98%

Icilin-evoked behavioral stimulation is attenuated by alpha2-adrenoceptor activation

et al. 2011

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Icilin is a transient receptor potential cation channel subfamily M (TRPM8) agonist that produces behavioral activation in rats and mice. Its hallmark overt pharmacological effect is wet-dog shakes (WDS) in rats. The vigorous shaking associated with icilin is dependent on NMDA receptor activation and nitric oxide production, but little else is known about the biological systems that modulate the behavioral phenomenon. The present study investigated the hypothesis that alpha2-adrenoceptor activation inhibits icilin-induced WDS. Rats injected with icilin (0.5, 1, 2.5, 5 mg/kg, i.p.) displayed dose-related WDS that were inhibited by pretreatment with a fixed dose of clonidine (0.15 mg/kg, s.c.). Shaking behavior caused by a fixed dose (2.5 mg/kg) of icilin was also inhibited in a dose-related manner by clonidine pretreatment (0.03–0.15 mg/kg, s.c.) and reduced by clonidine posttreatment (0.15 mg/kg, s.c.). Pretreatment with a peripherally restricted alpha2-adrenoceptor agonist, ST91 (0.075, 0.15 mg/kg), also decreased the incidence of shaking elicited by 2.5 mg/kg of icilin. Pretreatment with yohimbine (2 mg/kg, i.p.) enhanced the shaking induced by a low dose of icilin (0.5 mg/kg). The imidazoline site agonists, agmatine (150 mg/kg, i.p.) and 2-BFI (7 mg/kg, i.p.), did not affect icilin-evoked shaking. These results suggest that alpha2-adrenoceptor activation inhibits shaking induced by icilin and that increases in peripheral, as well as central, alpha2-adrenoceptor signaling oppose the behavioral stimulant effect of icilin.

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“…In antagonist experiments (idazoxan, prazosin, propranolol, naloxone), the antagonist drug was injected sc, 5 min before CRL41405. The doses of antagonists were chosen as follows from results obtained in our laboratory o n pancreatic secretion in rats: idazoxan 0.3 mgkg sc, an alpha-2-blocking dose validated against clonidine (Chariot et al, 1988); prazosin 1 mgkg sc, the largest alpha-1-blocking dose tolerated in our conditions (Nagain ct al. 1991); propranolol 1 mg/kg sc.…”

Section: Collection Of Puncrearic Juice and Experirrrentul Sclrcdulesmentioning

confidence: 99%

CRL41405: a drug with a new pharmacological profile on pancreatic exocrine secretion in the rat

Nagain

Chariot

Vaille

et al. 1992

Fundamemntal Clinical Pharma

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The recently described compound CRL41405 displays central effects suggesting possible antidepressive and awakening properties. In order to further analyze the pharmacology of this compound, its effects were studied on basal and stimulated pancreatic secretion in anaesthetized rats. CRL41405 alone (7-20 mg/kg, sc) had no effect on basal pancreatic secretion. Larger doses (67-200 mg/kg) increased basal secretion through the stimulation of cholinergic muscarinic receptors, the effect being antagonized by atropine. CRL41405 (20 mg/kg) suppressed the 2-deoxyglucose-induced (but not the acetylcholine-induced) stimulation of pancreatic secretion through an alpha-2 adrenoceptor inhibitory mechanism that was blocked by idazoxan (0.3 mg/kg, sc). In addition, a beta adrenoceptor mediated stimulation of sodium and bicarbonate excretion (blocked by propranolol) was evidenced when the alpha-2 inhibition was suppressed by idazoxan. Under alpha-2 adrenoceptor blockade, water and electrolyte stimulation by CRL41405 could be demonstrated on basal, 2-deoxyglucose-induced and acetylcholine-induced pancreatic secretion. This original profile makes CRL41405 a unique drug in pancreatic pharmacology.

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Central and peripheral inhibition of exocrine pancreatic secretion by alpha-2 adrenergic agonists in the rat

Cited by 12 publications

References 7 publications

Regulation of Pancreatic Secretion

Regulation of Pancreatic Secretion

Icilin-evoked behavioral stimulation is attenuated by alpha2-adrenoceptor activation

CRL41405: a drug with a new pharmacological profile on pancreatic exocrine secretion in the rat

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