Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion

Algazi, M. C.; Chen, Haw-Shi; Koss, Michael A.; Hogan, D. L.; Steinbach, Joseph H.; Pandol, Stephen; Isenberg, J. I.

doi:10.1152/ajpgi.1989.256.5.g833

Cited by 11 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The specificity of the VIP receptor for VIP could be confirmed in Peptide Hormone Receptors in Duodenocytcs vivo by use of the VIP antagonist [D-p-ClPHe6.Leul7]VIP, which completely inhibit ed VIP-induced bicarbonate secretion. Simi lar results were obtained by Algazi et al [19], In isolated hcpatocytes. the effect of gluca gon was mediated via stimulation of AC [20].…”

Section: Discussionsupporting

confidence: 65%

Bicarbonate Secretion in the Guinea Pig Duodenum: Functional Characterization of Peptide Hormone Receptors in Duodenal Enterocytes

et al. 1996

View full text Add to dashboard Cite

To get information about the peptide hormone receptors involved in duodenal bicarbonate secretion (DBS) and their cellular location, we determined DBS and adenylate cyclase (AC) activity in response to hormones of the vasoactive intestinal polypeptide (VΙP)/secretin family of peptides. DBS was determined in an isolated, perfused (24 mmol/l NaHCO₃) loop of the proximal duodenum in urethane- and indometacin-treated guinea pigs. AC stimulation was measured in isolated, homogenized duodenal enterocytes, the histological evaluation of which revealed their villous origin. VIP (10^–9 to 10^–7 mol × kg^–1) dose-dependently increased DBS 3.5-fold (p < 0.01); this effect was completely inhibited by the VIP antagonist [D-p-Cl-Phe6, Leul 7]VIP (10^–6 mol × kg^–1). Glucagon (10^–8 to 10^–6 mol × kg^–1) increased DBS 2.1-fold, while secretin (10^–9 to 10^–6 mol × kg^–1) had no effect on DBS, but stimulated pancreatic bicarbonate secretion. VIP concentra-tion-dependently increased AC activity 5.6-fold with an EC₅₀ of 1.3 × 10^–9 mol/l. [ D-p-Cl-Phe6, Leul 7] VIP caused a right-ward shift of the VIP concentration-response curve. A Schild plot analysis yielded a slope of 0.85 ± 0.11, indicating competitive inhibition. While secretin also stimulated AC activity, although 1,000-fold less potent than VIP, glucagon was ineffective. These data indicate that specific VIP receptors, which mediate VIP-stimulated bicarbonate secretion, are present on villous enterocytes. Stimulation of AC by secretin seems to be of pharmacological relevance only and is consistent with the lack of effect of this hormone on DBS. Glucagon likely activates a second transmitter of bicarbonate secretion, or works independently of AC.

show abstract

Section: Discussionsupporting

confidence: 65%

Bicarbonate Secretion in the Guinea Pig Duodenum: Functional Characterization of Peptide Hormone Receptors in Duodenal Enterocytes

et al. 1996

View full text Add to dashboard Cite

show abstract

“…Intravenous administration of the gastrointestinal peptides neurotensin and VIP and intraluminal perfusion of the duodenum with a PGEI analogue and HCl increased bicarbonate secretion, extending previous observations in restrained or anesthetized rats (2,(28)(29)(30), conscious dogs (4), and humans (1). Intraluminal PGs and circulating neurotensin and VIP stimulate duodenal bicarbonate secretion by distinct mechanisms (4, 28-30) and intraluminal HCO stimulates bicarbonate secretion via a PG-and VIP-dependent mechanism (2,30).…”

Section: Discussionsupporting

confidence: 82%

“…Intraluminal PGs and circulating neurotensin and VIP stimulate duodenal bicarbonate secretion by distinct mechanisms (4, 28-30) and intraluminal HCO stimulates bicarbonate secretion via a PG-and VIP-dependent mechanism (2,30). Therefore, the peripheral transmitters (i.e., NE and vasopressin) released in response to cerebroventricular CGRP probably interfere with each of these mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Cerebroventricular calcitonin gene-related peptide inhibits rat duodenal bicarbonate secretion by release of norepinephrine and vasopressin.

Brown¹

1990

J. Clin. Invest.

View full text Add to dashboard Cite

Proximal duodenal bicarbonate secretion is an important factor in humans and animals protecting the mucosa against acidpeptic damage. This study examined the mechanisms responsible for the central nervous system regulation of duodenal bicarbonate secretion by calcitonin gene-related peptide (CGRP) in unrestrained rats. Cerebroventricular administration of rat CGRP significantly inhibited basal duodenal bicarbonate secretion as well as the stimulatory effects of vasoactive intestinal peptide, neurotensin, a luminal PGEI analogue, misoprostol, and hydrochloric acid. The inhibitory effects of cerebroventricular CGRP were abolished by ganglionic blockade with chlorisondamine, significantly attenuated by noradrenergic blockade with bretylium, and enhanced by vagotomy. Inhibition of duodenal bicarbonate secretion induced by CGRP coincided with significant increases in plasma norepinephrine (NE) and vasopressin concentrations. The alpha adrenergic receptor antagonist, phentolamine, and the vasopressin VI receptor antagonist, (1-deaminopenicillamine, 2-[0-methyljTyr, 8-Arg)-vasopressin, given intravenously reversed the central inhibitory effect of CGRP by -50% each. Pretreatment of the animals with both phentolamine and the vasopressin antagonist completely abolished the central inhibitory effect of CGRP. Peripheral vasopressin and NE significantly decreased duodenal bicarbonate secretion, and their inhibitory effects were additive and prevented by phentolamine and the vasopressin antagonist, respectively. We conclude that cerebroventricular CGRP inhibits rat duodenal bicarbonate secretion by activation of sympathetic efferents and subsequent release of NE and vasopressin that act on alpha adrenergic and vasopressin receptors, respectively. (J. Clin. Invest. 1990. 85:25-32.) autonomic nervous system * brain-gut axis * calcitonin gene-related peptide * duodenal bicarbonate secretion * neuropeptides-vasopressin

show abstract

“…At least one of the neurons is cholinergic as judged by the effects of hexamethonium on fluid and alkaline secretion. Since atropine is without effect on fluid and bicarbonate secretion, the neurotransmitter at the effector cells in the crypts is non‐cholinergic, possibly involving vasoactive intestinal polypeptide (VIP; Cassuto et al 1981a , Algazi et al 1989 ). There are, however, observations reported in the literature to suggest that there is also a cholinergic influence on the cells producing the alkaline secretion, at least in some species.…”

Section: Discussionmentioning

confidence: 99%

Nervous control of alkaline secretion in the duodenum as studied by the use of cholera toxin in the anaesthetized rat

Jaup

Peregrin

Jodal

et al. 1998

Acta Physiologica Scandinavica

View full text Add to dashboard Cite

There is experimental evidence for an axon reflex control of alkaline secretion in the rat duodenum. We have investigated if there is also an intramural reflex control of alkaline secretion similar to that demonstrated with regard to the control of the fluid transport in the rat jejunum. Alkaline secretion in the duodenum of an anesthetized rat was continuously monitored using an in situ titration technique. The segment was extrinsically denervated. Exposing the duodenal segment to 80 microg cholera toxin markedly increased alkaline secretion. This response was abolished by hexamethonium (28 micromol (10 mg) kg(-1) body wt), a nicotinic receptor blocker, lidocaine (0.5 mL of a 1% solution on the serosal surface), a local anaesthetic, and nifedipine (5.75 micromol (2 mg) kg(-1) body wt i.v.), a calcium channel blocker. The response to cholera toxin was partially abolished by granisetron (0.11 micromol (40 microg) kg(-1) body wt i.v.), a 5-HT3 receptor blocker. Atropine (1.7 micromol (0.5 mg) kg(-1) body wt i.v.), a muscarinic receptor blocker, had no effect. We therefore conclude that the alkaline secretion in the rat jejunum evoked by cholera toxin exhibits the same pharmacological properties as the fluid secretion caused by the toxin in the jejunum. This suggests that the alkaline secretion in the rat duodenum is controlled not only by an axon reflex but also by an intramural secretory reflex similar to that controlling fluid transport in the rat jejunum.

show abstract

Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion

Cited by 11 publications

References 0 publications

Bicarbonate Secretion in the Guinea Pig Duodenum: Functional Characterization of Peptide Hormone Receptors in Duodenal Enterocytes

Bicarbonate Secretion in the Guinea Pig Duodenum: Functional Characterization of Peptide Hormone Receptors in Duodenal Enterocytes

Cerebroventricular calcitonin gene-related peptide inhibits rat duodenal bicarbonate secretion by release of norepinephrine and vasopressin.

Nervous control of alkaline secretion in the duodenum as studied by the use of cholera toxin in the anaesthetized rat

Contact Info

Product

Resources

About