Gastric Acid Secretion, Calcitonin and Secondary Hyperparathyroidism in Uremic Patients Undergoing Regular Dialysis Therapy (RDT)

1978 ◽  
Vol 1 (6) ◽  
pp. 260-265 ◽  
Author(s):  
F. Antonucci ◽  
P. Vezzadini ◽  
M. Cecchettin ◽  
G. Bonora ◽  
A. Adami ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Protective Factor ◽  
Serum Levels ◽  
Significant Negative Correlation ◽  
Inhibitory Effect ◽  
Negative Influence ◽  
Positive Influence ◽  
Uremic Patients

Fortyseven uremic patients on RDT underwent a gastric secretion study and a contemporary evaluation of serum levels of Calcium (Ca), Phosphate (iP), Magnesium (Mg), Alkaline Phosphatase (AP), immunoreactive gastrin (Gas), parathyroid hormone (PTH), calcitonin (CT). Secretory test (pentagastrin 6 μg/kg) was performed in the morning, after 12 hours of fasting, in the interdialytic interval. Female patients, male patients on RDT from less 1 year and hyposecretor patients were excluded from the study. On the basis of these criteria 25 normal or hyper-secretor males between 20 and 55 years old were selected. A significant positive correlation was found between PTH and CT, while a negative significant correlation was found between CT and BAO and CT and PAO. Similarly, a significant negative correlation was found between PTH and BAO and PTH and PAO. Multiple regression study showed that the negative influence of CT on BAO and PAO is more relevant than the positive influence of PTH. These data suggest that PTH and CT are involved in gastric acid secretion in uremia. Since the inhibitory effect of CT is prevailing on the stimulating effect of PTH, patients with higher levels of PTH and CT have a lower gastric acid secretion. CT might therefore be considered as a protective factor against hypersecretion in uremia.

Stimulation of neurons in rat ARC inhibits gastric acid secretion via hypothalamic CRF1/2- and NPY-Y1 receptors

2003 ◽  
Vol 285 (6) ◽  
pp. G1075-G1083 ◽  
Author(s):  
Johannes J. Tebbe ◽  
Silke Mronga ◽  
Martin K.-H. Schäfer ◽  
Jens Rüter ◽  
Peter Kobelt ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Excitatory Amino Acid ◽  
Inhibitory Effect ◽  
Receptor Subtypes ◽  
Npy Receptor ◽  
Y1 Receptors ◽  
Open Question

Neuropeptide Y (NPY) neuronal projections from the arcuate nucleus (ARC) have been proposed to target corticotropin-releasing factor (CRF)-positive neurons in the paraventricular nucleus (PVN) as part of the ARC-PVN axis. The existence of a positive feedback loop involving CRF receptors in the PVN has been suggested. Exogenous NPY and CRF in the PVN have been shown to inhibit gastric acid secretion. Recently, we have demonstrated that activation of ARC neurons inhibits gastric acid secretion via vagal pathways. To what extent NPY- and CRF-mediated mechanisms in the PVN contribute to the CNS modulation of gastric acid secretion is still an open question. In the present study, we performed consecutive bilateral microinjections of antagonists to NPY receptor subtypes Y1 and Y2 and to CRF1/2 receptors in the PVN and of the excitatory amino acid kainate in the ARC to assess the role of NPY- and CRF-mediated mechanisms in the kainate-induced effects on gastric acid secretion. Gastric acid secretion was measured at the basal condition and during pentagastrin (16 μg/kg body wt) stimulation. Microinjection of vehicle in the PVN and kainate in the ARC decreased gastric acid secretion. Microinjection of the specific NPY-Y1 receptor antagonist BIBP-3226 (200 pmol) and the nonspecific CRF1/2 antagonist astressin (30 pmol) in the PVN abolished the inhibitory effect of neuronal activation in the ARC by kainate on gastric acid secretion. The CRF antagonist astressin was more effective. Pretreatment with the NPY-Y2 receptor antagonist BIIE-0246 (120 pmol) in the PVN had no significant effect. Our results indicate that activation of neurons in the ARC inhibits gastric acid secretion via CRF1/2 and NPY-Y1 receptor-mediated pathways in the PVN.

Cholecystokinin inhibits gastric acid secretion through type "A" cholecystokinin receptors and somatostatin in rats

1992 ◽  
Vol 263 (3) ◽  
pp. G287-G292 ◽  
Author(s):  
K. C. Lloyd ◽  
H. E. Raybould ◽  
J. H. Walsh
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Type A ◽  
Inhibitory Effect ◽  
Cck Receptors ◽  
Cholecystokinin Receptors ◽  
Maximum Inhibition ◽  
Vagal Reflex ◽  
Dependent Pathway

The purpose of this study was to determine whether selective antagonism of type "A" cholecystokinin (CCK) receptors blocks inhibition of gastric acid secretion produced by CCK and whether this inhibition is mediated through either a somatostatin-dependent pathway or a vago-vagal reflex. Intravenous infusion of CCK (0.04-10 nmol.kg-1.h-1) dose dependently inhibited pentagastrin-stimulated gastric acid secretion in urethan-anesthetized rats, with a 50% inhibitory dose of 0.9 nmol.kg-1.h-1 and a maximum inhibition of approximately 50%. Blockade of type A CCK receptors using the selective type A receptor antagonist MK-329 completely reversed the inhibitory effect produced by a maximal dose (4 nmol.kg-1.h-1) of CCK. Immunoneutralization of endogenous somatostatin by administration of somatostatin monoclonal antibody abolished the inhibition produced by CCK. Concentrations of somatostatin in portal venous plasma were significantly increased after CCK administration; the increase in somatostatin was blocked by pretreatment with MK-329. In contrast, CCK-induced inhibition of gastric acid secretion was unaltered after perivagal capsaicin treatment. These results indicate that CCK inhibits gastric acid secretion in rats by activation of type A CCK receptors and through release of endogenous somatostatin.

Inhibitory effect of neurotensin on gastric acid secretion in rats

1990 ◽  
Vol 35 (4) ◽  
pp. 439-443 ◽  
Author(s):  
Robert A. Hammer ◽  
Richard E. Hernandez ◽  
Ann Shepard
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Effect
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