Physiology of gastric circulation

Guth, Paul H.; Leung, Felix W.; Kauffman, Gordon L.

doi:10.1002/cphy.cp060138

Cited by 19 publications

(32 citation statements)

References 178 publications

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“…However, it is difficult to exclude that part of the secreted somatostatin could pass into the capillary lumen and subse quently diffuse out to the gastrin cells located closer to the neck of the antral glands. The arrangement of the interglandular capillaries [28] would be consistent with such a view, which is also supported by the fact that a marked release of somatostatin to the blood stream can actually be demonstrated in re sponse to luminal acid. Furthermore, Kusumoto and Grube [29] in a study of rat antral endocrine cells reported that few of the soma tostatin cells had any particular relationship to the gastrin cells and that almost all of the pro cesses extended to capillaries rather than to gastrin cells.…”

Section: Discussionsupporting

confidence: 65%

Somatostatin Is an Essential Paracrine Link in Acid Inhibition of Gastrin Secretion

Holst¹,

Ørskov²,

Seier-Poulsen³

1992

Digestion

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We studied the functional coupling between antral somatostatin and gastrin cells in pigs using isolated perfused preparations of the antrum with intact supply of the vagus nerves. Luminal acidification significantly inhibited gastrin secretion to 61 ± 3 % of basal secretion and increased somatostatin output 9-fold. Intra-arterial infusion of somatostatin to concentrations of 10^-10 and 10^-9 mol/l inhibited gastrin secretion to 18 ± 9 and 33 ± 11 % of basal secretion. Electrical stimulation of the vagus nerves and intra-arterial infusion of gastrin-releasing polypeptide (GRP; 10^-9 mol/l) significantly increased both gastrin and somatostatin secretion. Addition to the perfusate of Fab fragments of somatostatin antibodies abolished the effect of somatostatin at 10^-10 mol/l and the acid inhibition of gastrin secretion, but had no effect on the response to vagus stimulation of GRP infusion. We conclude that a local release of somatostatin is essential for the acid-induced inhibition of gastrin secretion, whereas changes in the local somatostatin concentration are unlikely to play a major role in vagally or GRP-induced gastrin secretion.

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Section: Discussionsupporting

confidence: 65%

Somatostatin Is an Essential Paracrine Link in Acid Inhibition of Gastrin Secretion

Holst¹,

Ørskov²,

Seier-Poulsen³

1992

Digestion

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“…Increases in acid secretion induced by secretagogues (e.g., pentagastrin and histamine) can be associated with either an increase (187,390) or no change in blood flow (187,210,308,377). Conversely, inhibition of acid secretion (e.g., prostaglandins and somatostatin) can be associated with either an increase or decrease in gastric blood flow (186,308). Several potential reasons for the discordant observations have been offered, including the direct vasoactive properties of the secretagogues employed and prestimulation level of gastric blood flow (213).…”

Section: Stomach Postprandial Hyperemiamentioning

confidence: 94%

“…Based on the assumption that a metabolic mechanism would increase blood flow (oxygen delivery) during enhanced oxygen demand, numerous studies have addressed the relationship between gastric acid secretion and blood flow. These studies have yielded equivocal results (186,213). Some of the discrepancies have been attributed to the methods used to assess gastric blood flow.…”

Section: Stomach Postprandial Hyperemiamentioning

confidence: 94%

“…Some of the discrepancies have been attributed to the methods used to assess gastric blood flow. For example, the aminopyrine clearance technique is based on the pH partition of the probe and as such its clearance is increased during acid secretion, irrespective of the actual blood flow through the mucosa (186,213). Even with more reliable techniques for measuring blood flow, the relationship between gastric acid secretion and blood flow remains somewhat ambiguous.…”

Section: Stomach Postprandial Hyperemiamentioning

confidence: 99%

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The Gastrointestinal Circulation: Physiology and Pathophysiology

Granger

Holm

Kvietys

2015

Comprehensive Physiology

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The gastrointestinal (GI) circulation receives a large fraction of cardiac output and this increases following ingestion of a meal. While blood flow regulation is not the intense phenomenon noted in other vascular beds, the combined responses of blood flow, and capillary oxygen exchange help ensure a level of tissue oxygenation that is commensurate with organ metabolism and function. This is evidenced in the vascular responses of the stomach to increased acid production and in intestine during periods of enhanced nutrient absorption. Complimenting the metabolic vasoregulation is a strong myogenic response that contributes to basal vascular tone and to the responses elicited by changes in intravascular pressure. The GI circulation also contributes to a mucosal defense mechanism that protects against excessive damage to the epithelial lining following ingestion of toxins and/or noxious agents. Profound reductions in GI blood flow are evidenced in certain physiological (strenuous exercise) and pathological (hemorrhage) conditions, while some disease states (e.g., chronic portal hypertension) are associated with a hyperdynamic circulation. The sacrificial nature of GI blood flow is essential for ensuring adequate perfusion of vital organs during periods of whole body stress. The restoration of blood flow (reperfusion) to GI organs following ischemia elicits an exaggerated tissue injury response that reflects the potential of this organ system to generate reactive oxygen species and to mount an inflammatory response. Human and animal studies of inflammatory bowel disease have also revealed a contribution of the vasculature to the initiation and perpetuation of the tissue inflammation and associated injury response.

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“…While it is known that a decrease in gastric mucosal blood flow be low a critical level limits local oxygen deliv ery and decreases acid secretion, the con verse is not true, as increased mucosal blood flow does not augment acid secretion [23,24]. This suggests a supportive and permis sive role of mucosal blood flow in acid secre tion [25], PKC inhibitors are vasodilatory in the cerebral cirulation [26], However, this property, if present in the gastric circulation, should not predictably alter acid secretion [23,24], In contrast, PKC activators, such as phorbol esters, have vasoconstrictive proper ties in vivo which are reversed by staurosporine, a PKC inhibitor [27], With increasing doses of phorbol-12-13-dibutyrate between 5 and 5,000 ng/kg/min, arterial vasoconstric tion has been shown to increase progressive ly, whereas no effect was observed with PD [27], Although a nonspecific vascular effect of TPA might contribute to a decrease in acid secretion, the effective concentration of TPA in our study, 0.34 ng/kg/min, was 15-fold lower than the lowest dose used in the aforementioned study [27], Moreover, the blood pressure was unaffected by all com pounds utilized in our study.…”

Section: Discussionmentioning

confidence: 95%

Effects of Cyclic Adenosine Monophosphate-Dependent Protein Kinase and Calcium-Dependent Protein Kinase Modulators on Stimulated Gastric Acid Secretion in the Perfused Rat Stomach

Rotker

Strapko²,

Nandi³

et al. 1995

Pharmacology

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The effects of cyclic adenosine monophosphate-dependent protein kinase (PKA) and calcium-dependent protein kinase (PKC) modulators on secretagogue-stimulated gastric acid secretion were studied in the continuously perfused stomach of the anesthetized rat. Intravenous histamine (0.25 mg/kg/h) and pentagastrin (2 µg/kg/h) increased secretion above baseline by three- and fourfold, respectively. Parenteral administration of a PKC activator, 12-o-tetradecanoylphorbol-13-acetate (TPA; 0.1 nmol/h), decreased histamine- and pentagastrin-stimulated secretion by 64 and 40%, respectively. Administration of PKC inhibitors, calphostin C and 1-(5-isoquinolinyl sulfonyl)-2 methylpiperazine (H-7; 10 nmol/h, each), increased histamine- and pentagastrin-stimulated secretion by 115 and 74% and 42 and 79%, respectively, while equimolar concentrations (10 nmol/h) of three other isoquinoline sulfonamides (HA-1004, H-8, and H-89) had no effect, except for H-89 (100 nmol/h) which inhibited the histamine- and pentagastrin-stimulated acid secretion by 44%. Basal secretion was not significantly altered by the aforementioned drugs. The TPA-induced inhibition of pentagastrin-stimulated secretion was partially reversed by treatment with H-7. These findings support a role of PKA and PKC in the modulation of stimulated gastric acid secretion in vivo.

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Physiology of gastric circulation

Cited by 19 publications

References 178 publications

Somatostatin Is an Essential Paracrine Link in Acid Inhibition of Gastrin Secretion

Somatostatin Is an Essential Paracrine Link in Acid Inhibition of Gastrin Secretion

The Gastrointestinal Circulation: Physiology and Pathophysiology

Effects of Cyclic Adenosine Monophosphate-Dependent Protein Kinase and Calcium-Dependent Protein Kinase Modulators on Stimulated Gastric Acid Secretion in the Perfused Rat Stomach

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