Hormonal regulation of human lower esophageal sphincter competence: interaction of gastrin and secretin

Cohen, Sidney; Lipshutz, William

doi:10.1172/jci106512

Cited by 205 publications

(80 citation statements)

References 18 publications

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“…The most likely mechanism by which the pylorus serves this protective function would be the release of the duodenal hormones, secretin and cholecystokinin, in response to acidification. This would be analogous to the role of gastrin in maintaining lower esophageal sphincter competence (12)(13)(14). However, other hormonal or neural pathways can not be excluded.…”

Section: Discussionmentioning

confidence: 99%

“…The lower esophageal sphincter contracts in response to gastrin (12)(13)(14) whereas both the ileocecal (15) and choledochal sphincters (16) (25) and suggested that contaminants present in the GIH Research Unit preparation of cholecystokinin were not solely responsible for the observed response (26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

“…It has been presumed to be hormonal because the substances which were instilled into the duodenum are known to release both secretin and cholecystokinin (4)(5)(6)(7)(8)(9)(10)(11). In addition, a precedent for hormonal regulation of other gastrointestinal sphincters has been established (12)(13)(14)(15)(16). The purpose of this study is: (a) to utilize pyloric circular muscle, in vitro, to characterize the interaction of the gastrointestinal hormones on the pyloric sphincter; and (b) to relate these observations on pyloric muscle, in vitro, to studies carried out in man, in vivo.…”

Section: Introductionmentioning

confidence: 99%

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The Hormonal Regulation of Pyloric Sphincter Function

Fisher¹,

Lipshutz²,

Cohen³

1973

J. Clin. Invest.

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120

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A B S T R A C T The purpose of this study was to evaluate the hormonal control of pyloric sphincter function. Studies were performed on both pyloric circular muscle, in vitro, and the human pylorus, in vivo. Full dose-response curves to gastrin I, cholecystokinin, and secretin were constructed for the pyloric muscle of the opossum studied at its length of optimal tension development, Lo. Both cholecystokinin and secretin were potent agonists on the muscle but gastrin I gave no increase in muscle tension. The combination of cholecystokinin and secretin was additive at submaximal concentrations but potentiation of the maximal responses was not observed. Gastrin I produced a surmountable, competitive-like antagonism to the effect of cholecystokinin on the pyloric muscle. The octapeptide of cholecystokinin was a more potent agonist than the whole molecule of cholecystokinin on the pyloric muscle. In man, the pyloric pressure rose significantly during intravenous infusion of either cholecystokinin or secretin. The combination of maximal doses of both hormones did not show signficant potentiation. Gastrin I did not significantly increase pyloric pressure but did antagonize the pyloric response to duodenal acidification. These studies suggest that: (a) Both secretin and cholecystokinin augment pyloric sphincter pressure while gastrin I is an antagonist inhibiting their effects. (b) The hormonal responses of pyloric sphincter circular muscle, in vitro, can be correlated with human sphincter function, in vivo.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Hormonal Regulation of Pyloric Sphincter Function

Fisher¹,

Lipshutz²,

Cohen³

1973

J. Clin. Invest.

Self Cite

120

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“…Concerning the relationship between the rise in serum gastrin and LESP, exogenous gastrin such as gastrin 17 is capable to increase LESP but only in a pharmacologic dose (Cohen and Lipshutz 1971). Recently, it was reported, however, that gastrin 17 when administered in physiologic doses failed to increase LESP (Freeland et al 1976 ;Jennewein et al 1976).…”

Section: Discussionmentioning

confidence: 99%

The effect of increased gastrin release on lower esophageal sphincter pressure.

Watanabe

Sugawa

Hatafuku

et al. 1984

Tohoku J. Exp. Med.

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The present study was performed (1) to induce release of endogenous gastrin from the chronic isolated antrum, and (2) to note the effect of endogenous gastrin on lower esophageal sphincter pressure (LESP). Fifteen mongrel dogs weighing 15-20 kg were divided into 3 groups by the type of operation : 5 dogs with antral excision and B-II gastrojejunostomy (Group I) ; 5 dogs with a denervated antral pouch and B-II (Group IT); and 5 dogs with an innervated antral pouch and B-II (Group III). Fasting serum gastrin levels (SGL) and LESP were determined preoperatively (basal) and at 2 and 4 weeks postoperatively. SGL was measured by radioimmunoassay using an antibody to human gastrin I. LESP was determined by pullthrough technique using an assembly of 3 polyvinyl tubes perfused with water at 0.6 ml/min and connected to external transducers. The mean SGL at 2 and 4 weeks after operation in Group I and in Group II were not significantly different from basal SGL. The SGL rose significantly at 2 weeks and 4 weeks in Group III (p <0.05). The mean LESP at 2 and 4 weeks did not significantly change from the basal LESP in Group I, Group IT and Group III. The present data show that (1) increased endogenous gastrin was produced only in the presence of an innervated antral pouch, and (2) the increased gastrin level, however, did not affect LESP. lower esophageal sphincter ; endogenous gastrin ; innervated antral pouchThe physiologic role of gastrin in raising lower esophageal sphincter pressure (LESP) remains controversial. Though exogenous gastrin in a pharmacologic dose has been reported to increase LESP (Lipschutz and Cohen 1971), it is dubious that such gastrin has an effect on LESP in physiologic doses. As regards the effect of endogenous gastrin on LESP, previous studies have shown that an increase in LESP is produced by gastrin release during gastric alkalinization (Castell and Harris 1970). On the contrary, there is a conflicting data that LESP dose not correlate with serum gastrin levels and gastric alkalinization has been

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“…In recent years, there has been considerable investigation into the function of the esophagus and the lower esophageal sphincter (LES) ' in man and in animal models (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). These studies have described multiple mechanisms by which the esophagus and the LES responded to the various demands placed upon it.…”

Section: Introductionmentioning

confidence: 99%

The Mechanics of Esophageal Muscle Contraction. EVIDENCE OF AN INOTROPIC EFFECT OF GASTRIN

Cohen¹,

Green²

1973

J. Clin. Invest.

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A B S T R A C T To compare the mechanical properties of lower esophageal sphincter (LES) and esophageal circular smooth muscle, force-velocity determinations were made under various physiological conditions. Isotonic and isometric recordings of opossum circular muscle were used to obtain the velocity of shortening and force, respectively, during alterations in: (a) initial muscle length (preload), (b) afterload, (c) calcium concentration, and (d) gastrin I. Muscle contraction was elicited to the neurogenic response at the termination of electrical stimulation. A change in preload (muscle length) altered the peak force (Po) developed during an afterloaded contraction, but had only a minor effect on the maximum velocity of shortening (V max). At the length of optimal tension development, Lo, (preload, 1.5 g), the LES muscle had a V max of 6.1±0.2 mm/s and a Po of 17.7±0.7 g. The esophageal muscle at its Lo (preload, 2.0 g) had a V max of 6.3±0.5 mm/s and a Po of 18.1±1.2 g. A decrease in calcium from 2.5 mM to 1.0 mM significantly reduced the V max and Po of all muscle, but an increase in calcium to 5.0 mM increased these parameters only minimally. At a calcium of 1.0 mM, gastrin I increased both V max and Po of all muscle. This inotropic effect of gastrin I occurred at lower concentrations in LES muscle than in muscle from the upper esophagus. The power (force X velocity) and work (force X muscle shortening) of esophageal and LES muscle were calculated from these data. Both the work and power generated during esophageal and LES muscle contraction were determined by: (a) the initial muscle length as produced by the preload, (b) the afterload against which the muscle was contracting, and (c) the contractility of inotropism of the muscle, that is, the force-velocity curve on which the muscle was operating.

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Hormonal regulation of human lower esophageal sphincter competence: interaction of gastrin and secretin

Cited by 205 publications

References 18 publications

The Hormonal Regulation of Pyloric Sphincter Function

The Hormonal Regulation of Pyloric Sphincter Function

The effect of increased gastrin release on lower esophageal sphincter pressure.

The Mechanics of Esophageal Muscle Contraction. EVIDENCE OF AN INOTROPIC EFFECT OF GASTRIN

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