Effect of renal failure on gastrointestinal hormones

Hansky, J.

doi:10.1007/bf01556107

Cited by 19 publications

(10 citation statements)

References 28 publications

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“…Complete cessation of renal function after bilateral nephrectomy leads to elevated levels of a number of gastrointestinal hormones (Hansky 1979). Bilateral nephrectomy, as employed in the C. Post, unpublished data).…”

Section: Discussionmentioning

confidence: 95%

The effect of nephrectomy and ureter ligation on plasma neurotensin‐like immunoreactivity levels in the conscious rat

Theodorsson‐Norheim

Al‐Saffar

Saria

et al. 1985

Acta Physiologica Scandinavica

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The effect of nephrectomy and ureter ligation on the concentration of endogenous plasma neurotensin-like immunoreactivity (p-NTLI) was studied in conscious rats by means of antiserum 17-8201 which detects NT (1-13) only, and antiserum 0-7709 which detects NT(1-13) and NT(1-8). The unstimulated p-NTLI concentration did not change significantly during a 25-h observation period following nephrectomy in comparison with sham operation. However, stimulation of the release of NTLI by intraduodenal administration of oleic acid (0.2 ml) resulted in significantly higher p-NTLI levels in the nephrectomized rats than in the sham operated rats. Ureter ligation did not significantly affect basal or stimulated p-NTLI. The data indicate that the kidneys play an important part in the elimination of p-NTLI released after fat ingestion.

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Section: Discussionmentioning

confidence: 95%

The effect of nephrectomy and ureter ligation on plasma neurotensin‐like immunoreactivity levels in the conscious rat

Theodorsson‐Norheim

Al‐Saffar

Saria

et al. 1985

Acta Physiologica Scandinavica

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“…In a study on a large number of patients, it has been shown that the serum gastrin rises proportionally with the serum creatinine, the higher the creatinine, the higher the gastrin. The relationships of this increase in gastrin to acid secretion and peptic ulceration in this group ofpatients with chronic renal failure is not clear as most patients do not have ulcer problems (Hansky, 1979).…”

Section: Chronic Renalfailurementioning

confidence: 89%

Gastrins and gastrinomas

Hansky¹

1984

Postgraduate Medical Journal

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Summary The past 20 years have seen gastrin attain true hormonal status. Its structure has been characterized, it has been synthesized, radioimmunoassays for its measurement in blood and tissues have been developed and its physiology and metabolism elucidated. Of much interest to clinicians has been the association between gastrin and tumours of the pancreas (gastrinomas) and atrophic gastritis. The advent of gastrin measurement has facilitated the diagnosis of gastrinoma and the availability of powerful acid suppressants has altered the therapy of gastrinoma.

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“…In spite of the fact that there are considerable differences in the CCK B receptor expression depending on the species that were studied (Reubi et al 1997b), it seems reasonable to examine the presence of CCK B receptor and effects of gastrin also in the human kidney. Serum gastrin levels are high even in early stages of chronic renal failure (Hansky 1979), offering the possibility that gastrin and related hormones are involved in the structural remodelling of the kidney during the progression of renal disease (Wolf and Nielsen 1991). These potential effects of gastrin could also be of importance in other frequent conditions in which hypergastrinemia is observed such as Helicobacter pylori infection of the gastric mucosa (Graham et al 1991;Calam et al 1997) or during the therapeutically achieved suppression of gastric acid secretion (Sundler et al 1986;Lamberts 1993).…”

Section: Discussionmentioning

confidence: 99%

Evidence for CCKB receptors in the guinea-pig kidney: localization and characterization by [125I]gastrin binding studies and by RT-PCR

Schrenck

Weerth

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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Two types of receptors for gastrin and cholecystokinin (CCK) have been identified in the gastrointestinal tract and in the central nervous system: CCK(A) and CCK(B) receptors. Here we report evidence for the expression of CCK(B) receptors in the guinea-pig kidney. Specific binding sites for [125I]gastrin were detected in sections of the guinea-pig kidney: Binding was saturable, pH-, temperature- and time-dependent, and specific for gastrin-related peptides. The potencies for inhibition of binding of [125I]gastrin were CCK-8 > gastrin 17-I > CCK(B) receptor antagonist L-365,260 > des(SO3)CCK-8 > CCK(A) receptor antagonist L-364,718. Autoradiography demonstrated specific [125I]gastrin binding to medullary collecting ducts and to a much lesser extent to glomeruli, but not over other structures. CCK(B) receptor cDNA fragments were amplified by RT-PCR from total kidney, isolated tubuli and from tissues known to express CCK(B) receptors such as stomach and brain. The kidney might therefore be a previously unidentified site of action for gastrin and cholecystokinin-related peptides.

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Effect of renal failure on gastrointestinal hormones

Cited by 19 publications

References 28 publications

The effect of nephrectomy and ureter ligation on plasma neurotensin‐like immunoreactivity levels in the conscious rat

The effect of nephrectomy and ureter ligation on plasma neurotensin‐like immunoreactivity levels in the conscious rat

Gastrins and gastrinomas

Evidence for CCKB receptors in the guinea-pig kidney: localization and characterization by [125I]gastrin binding studies and by RT-PCR

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