The direct inhibition of pancreatic electrolyte secretion by noradrenaline in the isolated perfused cat pancreas.

Elisha, E. Eshaya; Hutson, D. H.; Scratcherd, T

doi:10.1113/jphysiol.1984.sp015233

Cited by 13 publications

(3 citation statements)

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“…Both inhibitory and excitatory actions have been reported (BABKIN et al, 1939;ELISHA et al, 1984). In this study, the increased response to antral distension after vagotomy alone was significantly smaller than that after vagotomy and splanchnicectomy.…”

Section: Discussionmentioning

confidence: 54%

Effects of antral distension on pancreatic exocrine secretion dogs: Evidence for a short reflex.

Furukawa

Okada

1987

Jpn.J.Physiol

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In WHITE et al. (1960) found that distension of the gastric corpus in conscious dogs caused an increase in pancreatic secretion via the vago-vagal reflex. DEGAS and YAMAGISHI (1978) reported that distension of the pyloric antrum in conscious dogs caused an increase in pancreatic secretion mainly through the vago-vagal reflex and partly through a rise in the serum gastrin concentration. DEGAS and YAMAGISHI (1978) stated that acid distension of the pyloric antrum caused no rise in pancreatic secretion after truncal vagotomy.The gastropancreatic reflexes have not been reported in anesthetized dogs or decerebrated dogs. Most anesthetics markedly diminish both the nervous activity and pancreatic response to a given stimulus. However, BABKIN (1924) has stated that chloralose is a very suitable narcotic for the study of the pancreatic secretion.

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Section: Discussionmentioning

confidence: 54%

Effects of antral distension on pancreatic exocrine secretion dogs: Evidence for a short reflex.

Furukawa

Okada

1987

Jpn.J.Physiol

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“…Finally, phenylephrine, which is considered as a specific a-agonist, did not stimulate amylase output from rat pancreatic fragments (Pearson et al 1984). A direct inhibitory effect of a-agonists upon fluid secretion has been reported in isolated, perfused rabbit (Hubel, 1970) and cat pancreas (Elisha et al 1984). In the present study, the a-stimulatory concentrations (from 10-6 to 10-4 M) of NA were without effect and the specific a-antagonist (both al and a2), phentolamine, did not change either the unstimulated amylase release or the dose-response curves for the stimulants and their electrophysiological effects.…”

Section: Effects Of Fl-agonistsmentioning

confidence: 88%

“…In vivo experiments have usually reported an inhibitory action of aor fi-agonists on protein secretion (Pfeffer & Hinton, 1956;Rudick, Gonda, Rosenberg, Chapman, Dreiling & Janowitz, 1973) or no effect at all (Roze, De la Tour, Chariot, Souchard, Vaille, Dupont, Jean & Wepierre, 1976;Furuta, Hashimoto & Washizaki, 1978;Demol & Sarles, 1980). In the case of inhibitory actions, it has been difficult to distinguish direct effects (due to activation ofreceptors located on the cell membrane) from indirect ones (due to vasoconstriction or an increase in vascular pressure) (Elisha, Hutson & Scratcherd, 1984). Moreover, during in vivo experiments, oc-agonists might act at both peripheral and central sites (Chariot, Roze, De la Tour, Souchard & Vaille, 1983).…”

Section: Introductionmentioning

confidence: 99%

Dopamine, noradrenaline and isoprenaline: secretory and electrophysiological effects in vitro on mouse pancreas.

Berger¹,

Laugier²

1986

The Journal of Physiology

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SUMMARY1. The amylase release from mouse pancreatic fragments was studied after dopamine (DA), and a-or f-sympathomimetic agonist application. The electrical parameters of the acinar cell membrane were also monitored.2. Both DA (from 5 x 10-6 to 10-4 M) and f-stimulants (isoprenaline from 5 x 10-6 to 5 x 1O-5 M; noradrenaline from 3 x 10-4 to 10-3 M) evoked an increase in amylase release, while noradrenaline in a-receptor stimulating doses failed to have any effect.3. The stimulatory effect of DA was blocked by ganglion blockers (Arfonad 10-5 M; pentamethonium 3 x 10-5 M) in a competitive manner and a dual antagonism was observed with atropine (10-7 M, 10-9 M). An a-receptor antagonist (phentolamine 1O-5 M) and a fl-receptor antagonist (propranolol 10-5 M) had no influence on the dopamine response. Moreover, the DA-induced stimulation was dependent on the presence of extracellular calcium. Perfusion with 10-4 and 10-3 M-DA or local application (from 77 /ug to 4-3 mg), resulted in marked membrane depolarization with diminution of the input resistance. This effect was blocked by atropine (10-5 M) and pentamethonium (10-4 M), but not by propranolol (10-5 M) or phentolamine (10-5 M).4. The isoprenaline-(IP) and noradrenaline-(NA) induced increase in amylase release was competitively blocked by propranolol (10-5 M) but not by phentolamine (10-5 M). Atropine caused a dose-dependent (10-7 M, 10-6 M) decrease in the maximal response (non-competitive antagonism), while the ganglion blocker pentamethonium (10-4 M) was without effect.5. NA caused membrane depolarization accompanied by a decrease in the input resistance after local application (from 77 jug to 1-6 mg). This effect persisted in the presence of 10-5 M-phentolamine but was abolished by 10-5 M-propranolol. IP perfusion (10-4 and 10-3 M) or local application (0 3 M; from 32 to 130 jug) caused the same electrical changes as those induced by NA and DA. The effect of IP persisted in the presence of 10-5 M-phentolamine, 10-4 M-pentamethonium and 10-4 Mdomperidone, but was abolished by propranolol (10-5 M) and tetrodotoxin (5 X 10-6 M) and markedly diminished by atropine (10-5 M). 6. The unstimulated amylase release from mouse pancreatic fragments was diminished in the presence of atropine (up to 40 % of the resting secretion) and ganglion blockers, but did not change significantly in the presence of either a-or fl-antagonists.Z. BERGER AND R. LAUGIER 7. It is concluded that: (a) the basal amylase release of this preparation is mainly regulated by cholinergic mechanisms, i.e. spontaneous acetylcholine liberation from nerve endings influenced by intrapancreatic ganglia. (b) DA and f-stimulants acting on their specific receptors induce an increase in pancreatic acinar cell membrane permeability. On the basis of competitive antagonism between DA and ganglion blockers, and dual antagonism between DA and atropine, the DA receptor is probably located before (or on) the intrapancreatic ganglion and connected to a post-ganglionic cholinergic fibre. The tetrodotoxin inhibition...

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Cholinergic and adrenergic control of enzyme secretion in isolated rat pancreas

1990

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While cholinergic nervous control of pancreatic enzyme secretion is well documented, data concerning adrenergic regulation of the exocrine pancreas are contradictory. In the present study we attempted to elucidate the direct action of adrenergic stimulation on pancreatic enzyme secretion. Rat pancreatic segments were set up in an organ bath and superfused with modified Krebs-Henseleit solution. Electrical field stimulation (EFS) stimulated amylase release from the segments. This stimulation was subject to inhibition with atropine up to 80%. Atropine-resistant enzyme discharge in response to EFS could be blocked by propranolol. Cholinergic agonist urecholine-induced amylase release was completely blocked by atropine. Noradrenaline (NA) exhibited a biphasic effect on amylase release. It inhibited the urecholine-induced amylase release in lower concentrations (10(-8)-10(-7) M), while it stimulated basal enzyme secretion in higher concentrations (10(-5)-10(-4) M). The inhibitory effect was mimicked by phenylephrine and completely prevented by prazosin. Isoprenaline concentration dependently enhanced, while clonidine and guanfacine did not affect amylase discharge. In conclusion, in rat pancreatic acinar tissue it seems likely that acetylcholine is the main neurotransmitter. Adrenergic action can be dual, inhibitory via alpha 1-adrenoceptors or stimulatory via beta-adrenoceptors on amylase secretion.

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The direct inhibition of pancreatic electrolyte secretion by noradrenaline in the isolated perfused cat pancreas.

Cited by 13 publications

References 13 publications

Effects of antral distension on pancreatic exocrine secretion dogs: Evidence for a short reflex.

Effects of antral distension on pancreatic exocrine secretion dogs: Evidence for a short reflex.

Dopamine, noradrenaline and isoprenaline: secretory and electrophysiological effects in vitro on mouse pancreas.

Cholinergic and adrenergic control of enzyme secretion in isolated rat pancreas

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