Brunner's Gland Secretion Research Articles

Neural pathways regulating Brunner's gland secretion in guinea pig duodenum in vitro

This study examined the neural pathways innervating Brunner's glands using a novel in vitro model of acinar secretion from Brunner's glands in submucosal preparations from the guinea pig duodenum. Neural pathways were activated by focal electrical stimulation and excitatory agonists, and videomicroscopy was used to monitor dilation of acinar lumen. Electrical stimulation of perivascular nerves evoked large dilations that were blocked by TTX (1 microM) or the muscarinic receptor antagonist 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride (1 microM). The nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium iodide (100 microM) had no effect, and the nerve-evoked responses were not inhibited by hexamethonium (200 microM). Dilations were abolished in preparations from chronically vagotomized animals. Activation of submucosal ganglia significantly dilated submucosal arterioles but not Brunner's glands. Effects of electrical stimulation of perivascular and submucosal nerves were not altered by guanethidine. Capsaicin and substance P also dilated arterioles but had no effect on Brunner's glands. Cholinergic (choline acetyltransferase-immunoreactive) nerve fibers were found in Brunner's glands. These findings demonstrate that Brunner's glands are innervated by cholinergic vagal fibers but not by capsaicin-sensitive or intrinsic enteric nerves.

A novel in vitro model of Brunner's gland secretion in the guinea pig duodenum.

A novel in vitro model that combined functional and morphological techniques was employed to directly examine pathways regulating Brunner's gland secretion in isolation from epithelium. In vitro submucosal preparations were dissected from guinea pig duodenum. A videomicroscopy technique was used to measure changes in luminal diameter of glandular acini as an index of activation of secretion. Carbachol elicited concentration-dependent dilations of the lumen (EC(50) = 2 microM) by activating muscarinic receptors on acinar cells. Ultrastructural and histological analyses demonstrated that dilation was accompanied by single and compound exocytosis of mucin-containing granules and the accumulation of mucoid material within the lumen. Inflammatory mediators (histamine, PGE(1), PGE(2)) and intestinal hormones (CCK, gastrin, vasoactive intestinal polypeptide, secretin) also stimulated glandular secretion, whereas activation of submucosal secretomotor neurons by 5-hydroxytryptamine did not. This study directly demonstrates that multiple hormonal, inflammatory, and neurocrine agents activate Brunner's glands, whereas many have dissimilar effects on the epithelium. This suggests that Brunner's glands are regulated by pathways that act both in parallel to and in isolation from those controlling epithelial secretion.

A novel in vitro model to examine mechanisms of Brunner's gland secretion in the guinea pig duodenum

A novel in vitro model to examine mechanisms of Brunner's gland secretion in the guinea pig duodenum

Effect of secretin and somatostatin on secretion of epidermal growth factor from brunner's glands in the rat

The effect of secretin and somatostatin on secretion of epidermal growth factor (EGF) from Brunner's glands was investigated in rats. Secretin increased volume secretion and the median output of EGF rose from 720 fmol/5 hr (total range 460-1320) in controls to 2065 fmol/5 hr (total range 1560-2730) at a dose of 50 pmol/kg/hr of secretin. Somatostatin inhibited Brunner's gland secretion, but the total output of EGF remained unchanged. Secretin-stimulated volume secretion and secretion of EGF was significantly reduced by simultaneous infusion of somatostatin. This study has shown that secretin stimulates secretion of EGF as well as volume secretion from Brunner's glands. Somatostatin prevents the effect of secretin on Brunner's glands, which suggests a role for somatostatin in control of Brunner's gland secretion.

Tolerance of rat duodenum to luminal acid

The tolerance of the duodenal mucosa to luminal acid was investigated by measuring with a liquid sensor pH microelectrode technique the epithelial surface pH (pHs) and subepithelial tissue pH (pHt) in rat proximal (duodenal bulb, Brunner gland area) and distal duodenum exposed to luminal acid. Under basal conditions, pHs was roughly equal in both parts of the duodenum; proximal duodenum, 7.40 +/- 0.14 (mean +/- SEM) at the villus tip and 7.54 +/- 0.16 at the depth of crypt; distal duodenum, 7.46 +/- 0.19 and 7.55 +/- 0.09, respectively. Yet, exposure of the mucosa to luminal acid (10 mM HCl) provoked a significantly lesser decrease of pHs (0.25 +/- 0.13 vs 0.42 +/- 0.12 pH units) in the proximal duodenum, suggesting that the response of epithelial HCO3 secretion to luminal acid is stronger in that part of the duodenum. Further, the initial acidification of pHs was followed in the proximal duodenum by a secondary alkalinization of pHs, leading to normalization of pHs, which may suggest activation of compensatory protective mechanisms. pHt at the villus tip was likewise roughly equal in both parts of duodenum (7.29 +/- 0.05 vs 7.17 +/- 0.04), but, again, acidification of the luminal perfusate progressively from 10 to 100 mM HCl induced a much earlier and significantly more profound acidification in the distal than in the proximal duodenum. The possible contribution of Brunner glands to the greater mucosal tolerance to acid in the proximal duodenum was assessed by investigating whether stimulation or inhibition of Brunner gland secretion modulates the response of the duodenal mucosa to acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of vasoactive intestinal polypeptide and somatostatin on secretion of epidermal growth factor and bicarbonate from Brunner's glands.

The effect of VIP and somatostatin on secretion of epidermal growth factor and bicarbonate from Brunner's glands was investigated in the rat. Vasoactive intestinal polypeptide infused in doses of 10 and 100 ng/kg/h significantly increased epidermal growth factor and bicarbonate output, but the concentrations did not change. Somatostatin infused at doses of 1, 10, 100 and 1000 ng/kg/h against a background of VIP 100 ng/kg/h inhibited in dose-dependent fashion the stimulated epidermal growth factor and bicarbonate outputs from rat Brunner's gland pouches. Also basal secretion was inhibited by somatostatin. Infusion of antisomatostatin serum stimulated Brunner's gland secretion. By immunohistochemical studies of rat duodena, it was found that epidermal growth factor, is almost exclusively present in the secretory cells of Brunner's glands. It is concluded that VIP stimulates secretion of epidermal growth factor and bicarbonate from Brunner's glands, an effect which is inhibited by somatostatin. A possible role for somatostatin in the control of Brunner's gland secretion is suggested.

Effect of secretin and glucagon on Brunner's gland secretion in the rat.

Brunner's gland secretion in response to infusion of secretin and glucagon was studied in the rat. Secretin was infused in doses of 15, 150 and 1500 ng/kg/h. All dose significantly increased bicarbonate and protein output and depleted Brunner's glands of PAS-positive mucin. Bicarbonate secretion was related to plasma secretin concentration, and a marked stimulatory effect of secretin was found in very low, probably physiological, plasma concentrations. Maximal bicarbonate output was obtained at a plasma concentration of secretin about 20 pmol/l. Glucagon was infused at a rate of 1.0 micrograms/kg/h and did not influence secretion rate or cell morphology. Also large doses of 5.0 and 50.0 micrograms/kg/h had no effect on Brunner's gland secretion. It is concluded that secretin in very low plasma concentrations stimulates secretion of bicarbonate, protein and mucus from Brunner's glands in the rat, while glucagon has no effect, and it is suggested that secretin may be involved in the physiological regulation of Brunner's gland secretion.

Mechanisms of the secretory and motor responses of the Brunner's gland region of the intestines to duodenal acidification.

The secretory and motor responses of the Brunner's gland region of the duodenum to luminal acidification were examined in rabbits anesthetized with urethan. Isomotic solutions of sodium chloride (pH 7.2) were perfused continuously through adjacent in situ segments. The pH of the perfusate of the proximal segment was changed to 2.0 for 30 min. Perfusion pressure (motor response) and volume and hexosamine concentration (secretory response) of the effluent were recorded for 3 h. The motor and secretory responses to luminal acidification were examined after intravenous (atropine) or intraluminal (lidocaine) pretreatment. Responses to intravenous infusions of serotonin or secretin were determined, also. Both atropine and lidocaine eliminated the initial motor and secretory responses of the proximal segment. Lidocaine eliminated the delayed secretory response of the distal segment. Serotonin caused initial motor and secretory responses, but secretin caused a delayed secretory response only. These results suggest that duodenal acidification elicits a two-phase increase in Brunner's gland secretion, the first being motor-dependent and the second motor-independent. The initial motor response was mediated by a local reflex composed of cholinergic and perhaps tryptaminergic receptors. The delayed secretory response was mediated by local and nonlocal, possibly hormonal, factors. Increased duodenal motility may provide a vehicle for the rapid expulsion of mucus, and thereby serve an important role in the function of the Brunner's glands.

Neural and hormonal control of Brunner's gland secretion

For many years it has been speculated that the physiological function of Brunner's glands was to secrete mucus to protect the proximal duodenum from the corrosive effects of acidified gastric juice. However the control of Brunner's gland secretion remains an enigma. Some evidence exists which indicates both cholinergic and adrenergic innervation of these glands, but current consensus weighs heavily in favor of a hormonal stimulus for glandular secretion. This is based in part on evidence obtained from denervated Brunner's gland pouches following a feeding stimulus. A number of hormones and hormone-like substances have been investigated as possible mediators in this secretory response, however, no specificity was ever demonstrated. The inability to pinpoint a given substance as a common mediator can be attributed to the fact that most active agents employed also affect duodenal motility. We present evidence that Brunner's gland secretion can be observed to be a diphasic response. The initial, transient response is always observed in the presence of increased duodenal motility. The sustained response does not require duodenal motility and is probably hormonally mediated.

Vasoactive Intestinal Polypeptidergic Nerves and Brunner's Gland Secretion in the Rat

Vasoactive intestinal polypeptide is known to have powerful effect on the secretions from endocrine and exocrine glands. By immunohistochemical studies on the rat, both a dense network of vasoactive intestinal polypeptide-immunoreactive nerve fibers around the acini of Brunner's glands, and small ganglia with vasoactive intestinal polypeptide-immunoreactive nerve-cell bodies close to the glands were demonstrated. Intravenous infusions of vasoactive intestinal polypeptide in doses of 10, 100, and 1000 ng/kg.h significantly increased flow rate, as well as bicarbonate and protein output from Brunner's glands in the rat. After infusion of vasoactive intestinal polypeptide the secretory cells, which in the control group were rich in PAS-positive mucin, became almost completely PAS-negative. It is suggested that physiologic secretion from Brunner's glands may be stimulated by the vasoactive intestinal polypeptidergic nerves.

The effect of glucagon on enterokinase secretion from Brunner's gland pouches in dogs.

ConclusionThe effects of glucagon on Brunner's gland secretion were studied in three mongrel dogs with pouches of the proximal duodenum. A continuous intravenous injection of glucagon given in a dose that produced maximal volume output caused sustained increases in volume, total protein, and enteropeptidase secretion from the pouches.

Glucagon stimulates Brunner's gland secretion.

GLUCAGON and secretin, chemical homologues having 14 similar amino-acids in identical positions1, induce choleresis2, stimulate insulin release3 and inhibit gastric secretion4. Glucagon, however, inhibits, while secretin stimulates, pancreatic fluid and electrolyte secretion5. Because three different preparations of secretin—synthetic porcine (Squibb), pure natural porcine (Jorpes and Mutt) and impure porcine (Boots)—stimulate Brunner's gland secretion6–8, we investigated whether glucagon would affect Brunner's gland secretion in dogs.

The hormonal control of Brunner's gland secretion and duodenal motility in the dog

The hormonal control of Brunner's gland secretion and duodenal motility in the dog

The effect of glucagon on Brunner's gland secretion in dogs.

SummaryPouches were prepared from the proximal duodenum in mongrel dogs and intravenous infusion of glucagon caused dose related increases in the volume of secretion from these pouches. The maximal response, 1.4 ml/15 min, was produced by a glucagon dose of 64 μg/kg-hr. Glucose infusions did not stimulate Brunner's gland secretion, indicating that the hyperglycemic effect of the glucagon was not responsible for the increase in duodenal secretion. Oral glucose administration also failed to stimulate Brunner's gland secretion.This work was supported by a Veterans Administration Clinical Investigator appointment (R.S.J.). The authors gratefully acknowledge the technical assistance of Elizabeth Stevenson. Dr. K. Jan Bossart kindly assisted in the surgical preparation of the animals used in this study. A portion of the glucagon used in this experiment was supplied by the Eli Lilly Company.

Effect of pure natural and synthetic secretion on Brunner's gland secretion in dogs.

Florey and Harding1,2 discovered the hormonal control of Brunner's gland secretion and suggested that secretin is the controlling hormone, but because their work was with an impure preparation the possibility remained that some hormone other than secretin was concerned. The name duocrinin was suggested for this hypothetical second hormone3.

Gastrointestinal hormones.

ArticlesGASTROINTESTINAL HORMONESM. I. GrossmanM. I. GrossmanPublished Online:01 Jan 1950https://doi.org/10.1152/physrev.1950.30.1.33MoreSectionsPDF (10 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe Origin and Understanding of the Incretin Concept16 July 2018 | Frontiers in Endocrinology, Vol. 9Gastrointestinal Hormones21 June 2018Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGBRobert E. Steinert, Christine Feinle-Bisset, Lori Asarian, Michael Horowitz, Christoph Beglinger, and Nori Geary21 December 2016 | Physiological Reviews, Vol. 97, No. 1The [pre-] history of the incretin conceptRegulatory Peptides, Vol. 128, No. 2Effects of cholecystokinin on the primate sphincter of oddiJournal of Surgical Research, Vol. 32, No. 1GASTRIC ACID, ULCERS, AND H2-RECEPTORSThe Lancet, Vol. 303, No. 7859Defeating the difficult duodenal dissectionThe American Journal of Surgery, Vol. 124, No. 1The hormonal control of Brunner's gland secretion and duodenal motility in the dogJournal of Surgical Research, Vol. 10, No. 9The influence of mammalian gastric stimulants on in vivo secretion of acid in frogsComparative Biochemistry and Physiology, Vol. 34, No. 3Digestive proteases in the holocephalian fish Chimaera monstrosa (L.)Comparative Biochemistry and Physiology, Vol. 31, No. 1Physiology of gastrinThe American Journal of Surgery, Vol. 117, No. 6Significance of vagal influences on release of antral gastrinThe American Journal of Surgery, Vol. 108, No. 1Comparison of the combined operation and Billroth I gastrectomy in the treatment of chronic duodenal ulcerThe American Journal of Surgery, Vol. 107, No. 2Acute pancreatitisThe American Journal of Medicine, Vol. 21, No. 2Exocrine pancreatic secretionThe American Journal of Medicine, Vol. 21, No. 1Small intestinal function in patients with an ileostomyThe American Journal of Medicine, Vol. 16, No. 2The problem of peptic ulcerThe American Journal of Medicine, Vol. 13, No. 5Fractionation of enterogastrone concentratesArchives of Biochemistry and Biophysics, Vol. 35, No. 2 More from this issue > Volume 30Issue 1January 1950Pages 33-90 https://doi.org/10.1152/physrev.1950.30.1.33PubMed15403661History Published online 1 January 1950 Published in print 1 January 1950 Metrics