Subcellular redistribution of AQP5 by vasoactive intestinal polypeptide in the Brunner's gland of the rat duodenum

Aquaporin (AQP)5, an exocrine-type water channel, was detected in the rat duodenum by Western blot analysis, and was localized by immunohistochemistry in the secretory granule membranes as well as in the apical and lateral aspects of the plasma membrane of Brunner's gland cells. Incubation of duodenal slices with vasoactive intestinal polypeptide (VIP) in vitro significantly increased the amount of AQP5 in the apical membrane fraction in a dose- and time-dependent manner with the amount reaching a plateau at 100 nM VIP and becoming near maximal after a 30-s incubation. Protein kinase inhibitors, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7, 50 μM), and N-[2-( p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89; PKA-specific, 1 μM) blocked this increase, but PKC-specific inhibitor calphostin C did not, implying the involvement of PKA but not PKC in this cellular event. Intravenous injection with VIP (40 μg/kg body wt) provoked dilation of the lumen of the Brunner's gland at 2 and 7 min and increased the staining intensity of AQP5 in the apical and lateral membranes. AQP1 (both nonglycosylated and glycosylated forms) was also found to localize in the apical and basolateral membranes of cells of Brunner's gland. VIP, however, did not provoke any significant change in the AQP1 level in the apical membrane, as judged from the results of the above in vitro and in vivo experiments. These results suggest that VIP induced the exocytosis of granule contents and simultaneously caused translocation of AQP5 but not of AQP1 to the apical membrane in Brunner's gland cells.

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Neural mediation of vasoactive intestinal polypeptide inhibitory effect on jejunal alanine absorption

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1998.275.4.g822 ◽

1998 ◽

Vol 275 (4) ◽

pp. G822-G828 ◽

Cited By ~ 6

Author(s):

K. A. Barada ◽

N. E. Saadé ◽

S. F. Atweh ◽

C. F. Nassar

Keyword(s):

Vasoactive Intestinal Polypeptide ◽

Myenteric Plexus ◽

Inhibitory Effect ◽

Dependent Manner ◽

Sham Control ◽

Extrinsic Innervation ◽

Myenteric Plexuses ◽

Intestinal Polypeptide

It was recently shown that vasoactive intestinal polypeptide (VIP) inhibits rat jejunal alanine absorption, an effect that was significantly reduced by vagotomy. This study assesses the role of capsaicin-sensitive primary afferents (CSPA) and the myenteric plexus in the inhibition of rat jejunal alanine absorption by VIP. Continuous intravenous infusion of VIP (11.2 ng ⋅ kg−1⋅ min−1) reduced alanine absorption by 60% in sham control rats and by 20% in rats neonatally treated with capsaicin ( P < 0.01). In in vitro experiments, VIP decreased alanine uptake by jejunal strips isolated from sham control rats in a dose-dependent manner. In the presence of 40 nM VIP, alanine uptake by full-thickness jejunal strips was reduced by 54% in sham control rats and by 25% in rats neonatally treated with capsaicin ( P < 0.001). On the other hand, VIP reduced alanine uptake by mucosal scrapings by 25% in sham rats compared with 9% reduction in neonatally treated rats. Chemical ablation of the extrinsic innervation and jejunal myenteric plexuses by pretreatment with benzalkonium chloride significantly ( P < 0.001) reduced basal alanine absorption and the inhibitory effect of VIP. Moreover, incubation of intestinal strips with tetrodotoxin and atropine reduced significantly ( P < 0.05) the inhibitory effect of VIP on alanine absorption. These data suggest that VIP exerts its inhibitory effect on alanine absorption through the CSPA fibers and the myenteric plexus. The neuronal circuitry of this inhibitory process may involve cholinergic muscarinic mechanisms.

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Vasoactive intestinal polypeptide regulation of rabbit renal adenylate cyclase activity in vitro.

The Journal of Physiology ◽

10.1113/jphysiol.1987.sp016558 ◽

1987 ◽

Vol 387 (1) ◽

pp. 1-17 ◽

Cited By ~ 15

Author(s):

N M Griffiths ◽

N L Simmons

Keyword(s):

Adenylate Cyclase ◽

Vasoactive Intestinal Polypeptide ◽

Cyclase Activity ◽

Adenylate Cyclase Activity ◽

Intestinal Polypeptide

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SCFA increase intestinal Na absorption by induction of NHE3 in rat colon and human intestinal C2/bbe cells

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.280.4.g687 ◽

2001 ◽

Vol 280 (4) ◽

pp. G687-G693 ◽

Cited By ~ 67

Author(s):

Mark W. Musch ◽

Cres Bookstein ◽

Yue Xie ◽

Joseph H. Sellin ◽

Eugene B. Chang

Keyword(s):

Brush Border ◽

Apical Membrane ◽

Bacterial Flora ◽

Short Chain Fatty Acids ◽

Rat Colon ◽

Dependent Manner ◽

Soluble Fiber ◽

Concentration Dependent Manner

Short-chain fatty acids (SCFA), produced by colonic bacterial flora fermentation of dietary carbohydrates, promote colonic Na absorption through mechanisms not well understood. We hypothesized that SCFA promote increased expression of apical membrane Na/H exchange (NHE), serving as luminal physiological cues for regulating colonic Na absorptive capacity. Studies were performed in human colonic C2/bbe (C2) monolayers and in vivo. In C2 cells exposed to butyrate, acetate, proprionate, or the poorly metabolized SCFA isobutyrate, apical membrane NHE3 activity and protein expression increased in a time- and concentration-dependent manner, whereas no changes were observed for NHE2. In contrast, no significant changes in brush-border hydrolase or villin expression were noted. Analogous to the in vitro findings, rats fed the soluble fiber pectin exhibited a time-dependent increase in colonic NHE3, but not NHE2, protein, mRNA, and brush-border activity. These changes were region-specific, as no changes were observed in the ileum. We conclude that luminal SCFA are important physiological cues for regulating colonic Na absorptive function, allowing the colon to adapt to chronic changes in dietary carbohydrate and Na loads.

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Participation of vasoactive intestinal polypeptide in ovarian steroids production during the rat estrous cycle and in the development of estradiol valerate-induced polycystic ovary

Reproduction ◽

10.1530/rep.1.01214 ◽

2007 ◽

Vol 133 (1) ◽

pp. 147-154 ◽

Cited By ~ 16

Author(s):

Claudio Parra ◽

Jenny L Fiedler ◽

S Leticia Luna ◽

Monika Greiner ◽

Vasantha Padmanabhan ◽

...

Keyword(s):

Estrous Cycle ◽

Vasoactive Intestinal Polypeptide ◽

Polycystic Ovary ◽

Secretory Activity ◽

Estradiol Valerate ◽

Steroid Secretion ◽

Cyclic Changes ◽

Intestinal Polypeptide

Vasoactive intestinal polypeptide (VIP) stimulates estradiol and progesterone release from ovarian granulosa cells in vitro. Very little information is available as to the role VIP plays in the control of steroid secretion during reproductive cyclicity and in ovarian pathologies involving altered steroid secretion. In this study, we determined the involvement of VIP in regulating ovarian androgen and estradiol release during estrous cyclicity and estradiol valerate (EV)-induced polycystic ovarian development in rats. Our findings show that androgen and estradiol release from ovaries obtained during different stages of rat estrous cycle mimic cyclic changes in steroid release observed in vivo with maximal release occurring during late proestrus. VIP increased androgen release from ovaries of all cycle stages except late proestrus and estradiol release from all cycle stages. Increases in VIP-induced androgen and estradiol release were maximal at early proestrus. Inclusion of saturating concentrations of androstenedione increased magnitude of VIP-induced estradiol release at diestrus and estrus but not proestrus. Magnitude of VIP-induced androgen and estradiol release tended to be greater in the ovaries from EV-treated rats with polycystic ovary compared with estrous controls. At the tissue level, ovarian VIP concentration was cycle stage dependent with highest level seen in diestrus. Maximum concentration of VIP was found in EV-treated rats. Changes in VIP were inversely related to changes in ovarian nerve growth factor, a neuropeptide involved in ovarian androgen secretion. These results strongly suggest that intraovarian VIP participates in the control of estradiol secretion during the rat estrous cycle and possibly in the maintenance of increased ovarian estradiol secretory activity of EV-treated rats.

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Reversal of nerve damage in streptozotocin-diabetic rats by acute application of insulin in vitro

Clinical Science ◽

10.1042/cs0750629 ◽

1988 ◽

Vol 75 (6) ◽

pp. 629-635 ◽

Cited By ~ 23

Author(s):

Geoffrey Burnstock ◽

Rhona Mirsky ◽

Abebech Belai

Keyword(s):

Vasoactive Intestinal Polypeptide ◽

Calcitonin Gene Related Peptide ◽

Diabetic Rats ◽

Diabetic Rat ◽

Rat Ileum ◽

Related Peptide ◽

Calcitonin Gene ◽

Enteric Nerves ◽

Intestinal Polypeptide

1. Immunohistochemical, immunoblotting and release experiments were performed on ileum from control rats, from 8-week streptozotocin-diabetic rats and from diabetic rats after acute application of insulin in vitro. 2. There was an increase in vasoactive-intestinal-polypeptide-like and a decrease in calcitonin-gene-related-peptide-like immunoreactivity in the myenteric plexus of the diabetic rat ileum, although electrically evoked release of both peptides from enteric nerves was defective. Acute application of insulin in vitro reversed the defective release and changes in immunoreactivity of vasoactive intestinal polypeptide and calcitonin-gene-related peptide seen in the enteric nerves of streptozotocin-diabetic rat ileum. 3. In addition, using a monoclonal neurofilament antibody RT 97 that recognizes a phosphorylated neurofilament epitope present in normal enteric nerves, it was shown that this phosphorylated neurofilament epitope was absent in diabetic nerves, even though a polyclonal neurofilament antibody revealed that neurofilaments were present in both axons and cell bodies of the myenteric plexus of diabetic rat ileum. After only 2 h of insulin incubation in vitro, the phosphorylated neurofilament epitope was again present in the nerves. 4. It is suggested that the abnormal distribution of phosphorylated neurofilaments and defective storage and release of vasoactive intestinal polypeptide and calcitonin-gene-related peptide in the present study may be a more general feature of diabetes. The restoration of these abnormalities by continuous acute insulin application in vitro shown here suggests that the availability of a steady level of insulin might prevent some of the changes which occur in early stages of diabetes. If so, this could influence the use of insulin in the treatment of diabetes, particularly in view of the recent report that short-term continuous subcutaneous insulin infusion restores the function of the autonomic and peripheral nerves in type I diabetic patients [Krönert, K., Hülsen, J., Luft, D., Stetter, T. & Eggstein, M. (1987) Journal of Clinical Endocrinology and Metabolism, 64, 1219–1223].

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