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Gastric Mucosal Receptors

Andrew H. Soll

10.1002/cphy.cp060210

Source: Supplement 17: Handbook of Physiology, The Gastrointestinal System, Neural and Endocrine Biology

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Dispersion, Separation, and Identification of Fundic Mucosal Cells
1.1 Dispersion of Gastric Cells
1.2 Cell Identification
1.3 Cell Separation
2 Background and Approaches for Studying Mucosal Cell Function
2.1 Parietal Cells
2.2 Endocrine Cells
2.3 Histamine Cells
2.4 Chief Cells
3 Receptors for Histamine
3.1 Parietal Cell Receptors
3.2 Receptor Specificity
3.3 Histamine Action on Nonparietal Cells
4 Gastrin Response and Gastrin Receptors
4.1 Canine Parietal Cells
4.2 Gastrin Receptors on Nonparietal Cells in Canine Fundic Mucosa
4.3 Histamine Release From Canine Fundic Mast Cells
4.4 Gastrin Action in Rabbit Gastric Glands and Frog Mucosa
4.5 Gastrin Receptors and Histamine Cells: Rabbit Fundic Mucosa
5 Cholinergic Receptors
5.1 Parietal Cell Muscarinic Receptors
5.2 Cholinergic Receptors on Nonparietal Cells
5.3 Muscarinic Receptor Subtypes
5.4 Muscarinic Receptors and Histamine Release
6 Receptors for Other Chemotransmitters
6.1 Prostaglandins and Parietal Cell Function
6.2 Receptors for Somatostatin
6.3 β‐Adrenergic Receptors
6.4 Adenosine Receptors
6.5 Epidermal Growth Factor
6.6 Enteroglucagon
7 Potentiating Interactions Between Secretagogues
7.1 Interactions at the Parietal Cell
7.2 Somatostatin Cell Interactions
8 Summary
Figure 1. Figure 1.

Gastrin binding to cell fractions separated by elutriation. Canine fundic mucosal cells were separated by elutriation into 9 fractions. Fraction 0 denotes mucosal cells before elutriation. Cell markers were quantitated on slides prepared by cytocentrifugation: toluidine blue staining for mast cells, periodic acid‐Schiff staining for mucous (PAS +) cells and parietal cells, and immunofluorescence for chief cells. Specific gastrin binding, expressed in fmol, of 125I‐labeled [Leu15]G‐17 specifically bound per 106 cells, was determined for these cell fractions. Nonsaturable binding was <15% of total binding in all fractions. Values are means for 4 preparations.

From Soll et al. 103
Figure 2. Figure 2.

Density‐gradient separation of small cell elutriator fraction. Linear density gradient was formed with bovine serum albumin and Ficoll in Sorvall zonal rotor. A: density of fractions and content of histamine, determined by radioenzymatic assay 105) and of mast cells, determined by toluidine blue staining of cytocentrifuge slides. B: on same gradient, cells were extracted for radioimmunoassay of somatostatin‐like and glucagon‐like immunoreactivity. Serotonin (5‐HT) activity determined by radioenzymatic assay and dopa decarboxylase activity by CO2 release method.

From Beaven et al. 8
Figure 3. Figure 3.

Effects of iodination with 127I on inhibition of 125I‐[Leu15]G‐17 binding by [Leu15]G‐17 and G‐17. Parietal cell‐enriched fraction was incubated in presence of 20 pM of 125I‐[Leu15]G‐17 and indicated concentrations of [Leu15]G‐17 and G‐17 and these 2 peptides after iodination with 127I.

From Soll et al. 103
Figure 4. Figure 4.

A: time course for association and dissociation of 125I‐[Leu15]G‐17 binding to elutriator‐enriched canine parietal cells. B: time course of specific and nonspecific (plus 1 μM pentagastrin) binding of 125I‐[Leu15]G‐17 to canine parietal cells at 37°C. For dissociation study, cells were also incubated in presence of 20 pM 125I‐[Leu15]G‐17 for 30 min at a cell concentration of 3 × 106/ml. Cell suspension was then diluted 100‐fold in presence and absence of excess unlabeled pentagastrin. Triplicate 5‐ml samples were centrifugea immediately and at indicated times of incubation. Values expressed as percentage of initial binding, determined immediately after dilution.

From Soil et al. 103
Figure 5. Figure 5.

Inhibition of 125I‐[Leu15]G‐17 binding and stimulation of aminopyrine (AP) accumulation by related peptides. A: binding of 125I‐[Leu15]G‐17 to parietal cells was determined in presence of indicated concentrations of G‐17, CCK‐8 and G‐14–17. Data have been expressed as specific tracer binding in fmol/106 cells at tracer concentration of 20 pM. B: effects of these same peptides on AP accumulation has been determined in presence of a histamine (10 nM) background. Data for CCK‐8 and G‐17 are mean ± SE for same 5 preparations illustrated in A. Data are expressed as percentage of response above 10 μM histamine background produced by 10 nM gastrin. Binding and functional studies were performed under identical conditions (Hank's balanced salt solution, 0.1% BSA (bovine serum albumin), and 25 nM HEPES buffer, with a 37°C, 30‐min incubation).

From Soil et al. 103
Figure 6. Figure 6.

Step density‐gradient separation of enriched parietal and chief cell elutriator fractions, performed with bovine serum albumin and Ficoll. Step density gradients were performed starting with elutriator fractions 6 and 7 (left panel) of fraction 8 (right panel). Two fractions were collected: fraction A cells at the interface above heavy step and fraction B cells that pelleted through this heavy solution. Percentage of parietal and chief cells in fractions and binding of 125I‐[Leu15]G‐17 expressed in fmol/106 cells. Values taken from 1 preparation; 3 other gradients yielded similar values.

From Soil et al. 103
Figure 7. Figure 7.

125I‐[Leu15]G‐17 receptors in small cell elutriator fraction: density‐gradient separation. Binding of 125I‐[Leu15]G‐17 was determined in a density gradient similar to that illustrated in Fig. 2, with data expressed in fmol/106 cells. Cells containing somatostatin‐like immunoreactivity (SLI) were quantitated with radioimmunoassay and data expressed in pmol/106 cells. Cells containing glucagon‐like and serotonin‐like immunoreactivity were identified with immunohistochemical techniques; values are expressed as percentage of total cells displaying specific immunoreactivity. In this experiment gastrin binding correlated with SLI content (r = 0.93).

From Soil et al. 102
Figure 8. Figure 8.

Effects of G‐17 and CCK‐8 on SLI release. SLI release was studied from small cell elutriator fraction (SCEF) placed in short‐term culture. Native heptadecapeptide gastrin (G‐17), cholecystokinin octapeptide (CCK‐8), and tetrapeptide of gastrin and CCK were added at beginning of 2‐h incubation period at indicated concentrations. Background of 1 μM epinephrine was used to amplify magnitude of SLI release; response to epinephrine alone is indicated at point corresponding to zero peptide concentration. Values expressed as percentage release of initial SLI cell content.

From Soil et al 101
Figure 9. Figure 9.

Binding of [3H]quinuclidinyl benzilate (QNB) to canine fundic cells. Binding of [3H]QNB was determined to indicated elutriator fractions of canine fundic mucosal cells. Values were corrected for protein content of each sample and expressed as percentage of maximal specific activity.

Adapted from Culp et al. 32
Figure 10. Figure 10.

Muscarinic receptor modulation of somatostatin release from canine fundic cells. Carbachol, in indicated concentrations, inhibited SLI release stimulated by combination of 1 μM epinephrine plus 10 nM gastrin. Atropine (A), studied at concentrations of 3.2–100 nM, produced progressive right shift of carbamylcholine (CARB) dose‐response curve. Values are expressed as percentage release of initial SLI content.

From Yamada et al. 116
Figure 11. Figure 11.

Adrenergic regulation of somatostatin release. Release of SLI from primary canine fundic cell cultures in response to epinephrine (E) was studied with (open circles) and without (closed circles) a background of 10 nM gastrin (G). Propranolol (0.1 and 1 μM) progressively shifted dose response to epinephrine plus gastrin to right (open squares and triangles). α‐Receptor antagonist phentolamine (10 μM) increased epinephrine response (closed triangles); specificity of receptor accounting for this effect was difficult to establish. Values are expressed as percentage of initial cell SLI content released.

From Yamada et al. 116
Figure 12. Figure 12.

Model for fundic mucosal regulatory pathways derived from studies with canine cells, outlining present view of receptors and pathways regulating parietal cell function. Histamine, gastrin, and acetylcholine (ACH) act in parallel on specific receptors on parietal cell, with their actions amplified by potentiating interactions. Gastrin, delivered by capillaries, also acts directly on receptors on somatostatin cell to activate an inhibitory pathway. Gastrin receptors are probably also present on stem cell and possible on other cell types, such as endocrine‐like cells. Histamine is delivered from mast cells located in lamina propria; canine fundic mast cells appear to have stimulatory adenosine and IgE receptors and inhibitory prostaglandin and β‐adrenergic receptors. Other potentially important mast cell receptors remain to be established. Acetylcholine is delivered by postganglionic nerves to muscarinic receptors on somatostatin cell that attenuate somatostatin release; thus acetylcholine dampens inhibitory pathway mediated by somatostatin. This double negative effect of acetylcholine at somatostatin cell—inhibition of an inhibitor—enhances acid secretory response. Muscarinic receptors on other cell types may also modulate acid secretory response and many factors may influence acetylcholine delivery, but these elements remain to be determined. Adrenergic (ADR) input inhibiting mast cell histamine and stimulating somatostatin release may be an important inhibitory pathway.

From Sanders and Soil 91a
Figure 13. Figure 13.

Speculation on balance of gastrin and CCK actions in canine fundic mucosa. Integration between pathways regulating acid secretion is shown through several mechanisms that may modulate final acid secretory response to opposing actions on CCK and gastrin on parietal and somatostatin cells. Acetylcholine inhibits SLI release in response to chemotransmitters but enhances parietal cell function; by both mechanisms acetylcholine shifts balance of gastrin action to acid‐stimulatory side. β‐Adrenergic agents enhance CCK and gastrin action on SLI release and impair delivery of histamine but appear to have no direct effect on canine parietal cell function. Thus by at least 2 mechanisms, β‐adrenergic agents shift balance of CCK/gastrin action to acid‐inhibitory side. In contrast, histamine influences only stimulatory limb, enhancing parietal cell response to gastrin and CCK‐8 but not influencing somatostatin release. Differences in receptor specificity for CCK and gastrin may also influence balance of actions of these peptides; CCK‐8 more potently stimulates SLI release than does gastrin, possibly accounting for impaired efficacy of this peptide as a stimulant of acid secretion in vivo in dogs.

From Soil et al. 101


Figure 1.

Gastrin binding to cell fractions separated by elutriation. Canine fundic mucosal cells were separated by elutriation into 9 fractions. Fraction 0 denotes mucosal cells before elutriation. Cell markers were quantitated on slides prepared by cytocentrifugation: toluidine blue staining for mast cells, periodic acid‐Schiff staining for mucous (PAS +) cells and parietal cells, and immunofluorescence for chief cells. Specific gastrin binding, expressed in fmol, of 125I‐labeled [Leu15]G‐17 specifically bound per 106 cells, was determined for these cell fractions. Nonsaturable binding was <15% of total binding in all fractions. Values are means for 4 preparations.

From Soll et al. 103


Figure 2.

Density‐gradient separation of small cell elutriator fraction. Linear density gradient was formed with bovine serum albumin and Ficoll in Sorvall zonal rotor. A: density of fractions and content of histamine, determined by radioenzymatic assay 105) and of mast cells, determined by toluidine blue staining of cytocentrifuge slides. B: on same gradient, cells were extracted for radioimmunoassay of somatostatin‐like and glucagon‐like immunoreactivity. Serotonin (5‐HT) activity determined by radioenzymatic assay and dopa decarboxylase activity by CO2 release method.

From Beaven et al. 8


Figure 3.

Effects of iodination with 127I on inhibition of 125I‐[Leu15]G‐17 binding by [Leu15]G‐17 and G‐17. Parietal cell‐enriched fraction was incubated in presence of 20 pM of 125I‐[Leu15]G‐17 and indicated concentrations of [Leu15]G‐17 and G‐17 and these 2 peptides after iodination with 127I.

From Soll et al. 103


Figure 4.

A: time course for association and dissociation of 125I‐[Leu15]G‐17 binding to elutriator‐enriched canine parietal cells. B: time course of specific and nonspecific (plus 1 μM pentagastrin) binding of 125I‐[Leu15]G‐17 to canine parietal cells at 37°C. For dissociation study, cells were also incubated in presence of 20 pM 125I‐[Leu15]G‐17 for 30 min at a cell concentration of 3 × 106/ml. Cell suspension was then diluted 100‐fold in presence and absence of excess unlabeled pentagastrin. Triplicate 5‐ml samples were centrifugea immediately and at indicated times of incubation. Values expressed as percentage of initial binding, determined immediately after dilution.

From Soil et al. 103


Figure 5.

Inhibition of 125I‐[Leu15]G‐17 binding and stimulation of aminopyrine (AP) accumulation by related peptides. A: binding of 125I‐[Leu15]G‐17 to parietal cells was determined in presence of indicated concentrations of G‐17, CCK‐8 and G‐14–17. Data have been expressed as specific tracer binding in fmol/106 cells at tracer concentration of 20 pM. B: effects of these same peptides on AP accumulation has been determined in presence of a histamine (10 nM) background. Data for CCK‐8 and G‐17 are mean ± SE for same 5 preparations illustrated in A. Data are expressed as percentage of response above 10 μM histamine background produced by 10 nM gastrin. Binding and functional studies were performed under identical conditions (Hank's balanced salt solution, 0.1% BSA (bovine serum albumin), and 25 nM HEPES buffer, with a 37°C, 30‐min incubation).

From Soil et al. 103


Figure 6.

Step density‐gradient separation of enriched parietal and chief cell elutriator fractions, performed with bovine serum albumin and Ficoll. Step density gradients were performed starting with elutriator fractions 6 and 7 (left panel) of fraction 8 (right panel). Two fractions were collected: fraction A cells at the interface above heavy step and fraction B cells that pelleted through this heavy solution. Percentage of parietal and chief cells in fractions and binding of 125I‐[Leu15]G‐17 expressed in fmol/106 cells. Values taken from 1 preparation; 3 other gradients yielded similar values.

From Soil et al. 103


Figure 7.

125I‐[Leu15]G‐17 receptors in small cell elutriator fraction: density‐gradient separation. Binding of 125I‐[Leu15]G‐17 was determined in a density gradient similar to that illustrated in Fig. 2, with data expressed in fmol/106 cells. Cells containing somatostatin‐like immunoreactivity (SLI) were quantitated with radioimmunoassay and data expressed in pmol/106 cells. Cells containing glucagon‐like and serotonin‐like immunoreactivity were identified with immunohistochemical techniques; values are expressed as percentage of total cells displaying specific immunoreactivity. In this experiment gastrin binding correlated with SLI content (r = 0.93).

From Soil et al. 102


Figure 8.

Effects of G‐17 and CCK‐8 on SLI release. SLI release was studied from small cell elutriator fraction (SCEF) placed in short‐term culture. Native heptadecapeptide gastrin (G‐17), cholecystokinin octapeptide (CCK‐8), and tetrapeptide of gastrin and CCK were added at beginning of 2‐h incubation period at indicated concentrations. Background of 1 μM epinephrine was used to amplify magnitude of SLI release; response to epinephrine alone is indicated at point corresponding to zero peptide concentration. Values expressed as percentage release of initial SLI cell content.

From Soil et al 101


Figure 9.

Binding of [3H]quinuclidinyl benzilate (QNB) to canine fundic cells. Binding of [3H]QNB was determined to indicated elutriator fractions of canine fundic mucosal cells. Values were corrected for protein content of each sample and expressed as percentage of maximal specific activity.

Adapted from Culp et al. 32


Figure 10.

Muscarinic receptor modulation of somatostatin release from canine fundic cells. Carbachol, in indicated concentrations, inhibited SLI release stimulated by combination of 1 μM epinephrine plus 10 nM gastrin. Atropine (A), studied at concentrations of 3.2–100 nM, produced progressive right shift of carbamylcholine (CARB) dose‐response curve. Values are expressed as percentage release of initial SLI content.

From Yamada et al. 116


Figure 11.

Adrenergic regulation of somatostatin release. Release of SLI from primary canine fundic cell cultures in response to epinephrine (E) was studied with (open circles) and without (closed circles) a background of 10 nM gastrin (G). Propranolol (0.1 and 1 μM) progressively shifted dose response to epinephrine plus gastrin to right (open squares and triangles). α‐Receptor antagonist phentolamine (10 μM) increased epinephrine response (closed triangles); specificity of receptor accounting for this effect was difficult to establish. Values are expressed as percentage of initial cell SLI content released.

From Yamada et al. 116


Figure 12.

Model for fundic mucosal regulatory pathways derived from studies with canine cells, outlining present view of receptors and pathways regulating parietal cell function. Histamine, gastrin, and acetylcholine (ACH) act in parallel on specific receptors on parietal cell, with their actions amplified by potentiating interactions. Gastrin, delivered by capillaries, also acts directly on receptors on somatostatin cell to activate an inhibitory pathway. Gastrin receptors are probably also present on stem cell and possible on other cell types, such as endocrine‐like cells. Histamine is delivered from mast cells located in lamina propria; canine fundic mast cells appear to have stimulatory adenosine and IgE receptors and inhibitory prostaglandin and β‐adrenergic receptors. Other potentially important mast cell receptors remain to be established. Acetylcholine is delivered by postganglionic nerves to muscarinic receptors on somatostatin cell that attenuate somatostatin release; thus acetylcholine dampens inhibitory pathway mediated by somatostatin. This double negative effect of acetylcholine at somatostatin cell—inhibition of an inhibitor—enhances acid secretory response. Muscarinic receptors on other cell types may also modulate acid secretory response and many factors may influence acetylcholine delivery, but these elements remain to be determined. Adrenergic (ADR) input inhibiting mast cell histamine and stimulating somatostatin release may be an important inhibitory pathway.

From Sanders and Soil 91a


Figure 13.

Speculation on balance of gastrin and CCK actions in canine fundic mucosa. Integration between pathways regulating acid secretion is shown through several mechanisms that may modulate final acid secretory response to opposing actions on CCK and gastrin on parietal and somatostatin cells. Acetylcholine inhibits SLI release in response to chemotransmitters but enhances parietal cell function; by both mechanisms acetylcholine shifts balance of gastrin action to acid‐stimulatory side. β‐Adrenergic agents enhance CCK and gastrin action on SLI release and impair delivery of histamine but appear to have no direct effect on canine parietal cell function. Thus by at least 2 mechanisms, β‐adrenergic agents shift balance of CCK/gastrin action to acid‐inhibitory side. In contrast, histamine influences only stimulatory limb, enhancing parietal cell response to gastrin and CCK‐8 but not influencing somatostatin release. Differences in receptor specificity for CCK and gastrin may also influence balance of actions of these peptides; CCK‐8 more potently stimulates SLI release than does gastrin, possibly accounting for impaired efficacy of this peptide as a stimulant of acid secretion in vivo in dogs.

From Soil et al. 101
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Article Title: Gastric Mucosal Receptors
 

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Andrew H. Soll. Gastric Mucosal Receptors. Compr Physiol 2011, Supplement 17: Handbook of Physiology, The Gastrointestinal System, Neural and Endocrine Biology: 193-214. First published in print 1989. doi: 10.1002/cphy.cp060210