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

Abstract

The amylase release from mouse pancreatic fragments was studied after dopamine (DA), and alpha- or beta-sympathomimetic agonist application. The electrical parameters of the acinar cell membrane were also monitored. Both DA (from 5 X 10(-6) to 10(-4) M) and beta-stimulants (isoprenaline from 5 X 10(-6) to 5 X 10(-5) M; noradrenaline from 3 X 10(-4) to 10(-3) M) evoked an increase in amylase release, while noradrenaline in alpha-receptor stimulating doses failed to have any effect. 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 alpha-receptor antagonist (phentolamine 10(-5) M) and a beta-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 micrograms 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). 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. NA caused membrane depolarization accompanied by a decrease in the input resistance after local application (from 77 micrograms 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 micrograms) 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) M-domperidone, but was abolished by propranolol (10(-5) M) and tetrodotoxin (5 X 10(-6) M) and markedly diminished by atropine (10(-5) M).(ABSTRACT TRUNCATED AT 400 WORDS)

• Authors: Z Berger, R Laugier
• Journal: The Journal of physiology (J Physiol) Vol. 376 Pg. 359-75 (Jul 1986) ISSN: 0022-3751 [Print] England
• PMID: 2432233 (Publication Type: Journal Article)

Chemical References

• Bis-Trimethylammonium Compounds
• Ganglionic Blockers
• Sympatholytics
• Tetrodotoxin
• pentamethonium
• Domperidone
• Atropine
• Amylases
• Isoproterenol
• Dopamine
• Norepinephrine

Topics

• Action Potentials (drug effects)
• Amylases (metabolism)
• Animals
• Atropine (pharmacology)
• Bis-Trimethylammonium Compounds (pharmacology)
• Domperidone (pharmacology)
• Dopamine (pharmacology)
• Dose-Response Relationship, Drug
• Ganglionic Blockers (pharmacology)
• In Vitro Techniques
• Isoproterenol (pharmacology)
• Male
• Mice
• Norepinephrine (pharmacology)
• Pancreas (physiology)
• Stimulation, Chemical
• Sympatholytics (pharmacology)
• Tetrodotoxin (pharmacology)
• Time Factors