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Query: UNIPROT:P61278 (
somatostatin
)
22,083
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The effects of a number of peptides which are found in the gastrointestinal tract have been ascertained on the direct current recorded dorsal and ventral root responses of the isolated hemisected toad spinal cord. Motilin, substance P,
bombesin
, neurotensin, and thyrotropin releasing hormone had potent depolarizing actions on dorsal root terminals and motoneurons. These substances evoked discernable effects at concentrations as low as 10--7 M, or even lower with motilin. The effects of motilin, neurotensin, and thyrotropin-releasing hormone were greatly reduced or abolished by perfusion of the preparation with tetrodotoxin. Adrenocorticotrophic hormone, secretin, and pancreozymin (cholecystokinin) also depolarized dorsal root terminals and motoneurons. The effects of secretin and cholecystokinin were not abolished by tetrodotoxin. Leu- and Met-enkephalin had weak hyperpolarizing actions on the dorsal and ventral root potentials of repetitively stimulated preparations. Gastrin, gastric inhibitory peptide, glucagon, and
somatostatin
had no apparent effects on the responses of the preparation. Angiotensin and vasopressin both had rather weak depolarizing effects on the dorsal and ventral roots.
...
PMID:Actions of various gastrointestinal peptides on the isolated amphibian spinal cord. 11 60
We have prepared (125)I-labeled [Tyr(4)]
bombesin
and have examined the kinetics, stoichiometry, and chemical specificity with which the labeled peptide binds to dispersed acini from guinea pig pancreas. Binding of (125)I-labeled [Tyr(4)]-
bombesin
was saturable, temperature-dependent, and reversible and reflected interaction of the labeled peptide with a single class of binding sites on the plasma membrane of pancreatic acinar cells. Each acinar cell possessed approximately 5000 binding sites, and binding of the tracer to these sites could be inhibited by [Tyr(4)]
bombesin
[concentration for half-maximal effect (Kd), 2 nM],
bombesin
(Kd, 4 nM), or litorin (Kd, 40 nM) but not by eledoisin, physalemin,
somatostatin
, carbachol, atropine, secretin, vasocative intestinal peptide, neurotensin, or bovine pancreatic polypeptide. At high concentrations (>0.1 muM), cholecystokinin and caerulein each caused a small (15-20%) reduction in binding of lableled [Tyr(4)]
bombesin
. With
bombesin
, litorin, and [Tyr(4)]
bombesin
, there was a close correlation between the relative potency for inhibition of binding of labeled [Tyr(4)]
bombesin
and that for stimulation of amylase secretion. For a given peptide, however, a 10-fold higher concentration was required for half-maximal inhibition of binding than for half-maximal stimulation of amylase secretion, calcium outflux, or cyclic GMP accumulation. These results indicate that dispersed acini from guinea pig pancreas possess a single class of receptors that interact with [Tyr(4)]
bombesin
,
bombesin
, and litorin and that occupation of 25% of these receptors will cause a maximal biological response.
...
PMID:Interaction of bombesin and litorin with specific membrane receptors on pancreatic acinar cells. 21 15
We have prepared 125I-labeled physalaemin and have examined the kinetics, stoichiometry, and chemical specificity with which the labeled peptide binds to dispersed acini from guinea pig pancreas. Binding of 125I-labeled physalaemin was saturable, temperature-dependent, and reversible and reflected interaction of the labeled peptide with a single class of binding sites on the plasma membrane of pancreatic acinar cells. Each acinar cell possessed approximately 500 binding sites, and binding of the tracer to these sites could be inhibited by physalaemin [concentration for half-maximal effect (Kd), 2 nM], substance P (Kd, 5 nM), or eledoisin (Kd, 300 nM) but not by cholecystokinin, caerulein,
bombesin
, litorin, gastrin, secretin, vasoactive intestinal peptide, glucagon,
somatostatin
, neurotensin, bovine pancreatic polypeptide, leucine-enkephalin, methionine-enkephalin, atropine, or carbamylcholine. With physalaemin, substance P, and eledoisin, there was a close correlation between the relative potency for inhibition of binding of labeled physalaemin and that for stimulation of amylase secretion. For a given peptide, however, a 3-fold higher concentration was required for half-maximal inhibition of binding than for half-maximal stimulation of amylase secretion, calcium outflux, or cyclic GMP accumulation. These results indicate that dispersed acini from guinea pig pancreas possess a single class of receptors that interact with physalaemin, substance P, and eledoisin and that occupation of 45% of these receptors will cause a maximal biological response.
...
PMID:Interaction of physalaemin, substance P, and eledoisin with specific membrane receptors on pancreatic acinar cells. 23 Apr 88
This is a review of current information concerning the role of hormones and the autonomic nervous system in the control of exocrine secretions of the pancreas. A greater emphasis has been placed on the role of hormones because of information accumulated during the last several years. With the development of radioimmunoassay techniques, it is now possible to correlate circulating hormone concentrations with biological function. The role of hormones has been discussed with the framework of the secretin-glucagon family, the cholecystokinin-gastrin family, and other proposed gastrointestinal hormones and related peptides. Gastrin, secretin and cholecystokinin-pancreozymin are three prime gut hormones that regulate pancreatic secretion. Other hormones that may have a role in pancreatic secretion include glucagon, vasoactive intestinal polypeptide, chymodenin,
somatostatin
, pancreatic polypeptide, motilin, and
bombesin
. Neural mechanisms play an important although not so succinct a role in the over-all control of exocrine secretion. A complex relationship exists between the parasympathetic nervous system and the release of the hormones and their effect on pancreatic acinar and duct cells.
...
PMID:Neurohormonal control of pancreatic secretion. A review. 34 Mar 22
The distribution of peptide hormone-like immunostaining in the gastrointestinal tract of 11 teleost species was investigated by immunofluorescence. Cells immunoreactive for
somatostatin
were found in the glandular epithelium of the stomach of four species and in the epithelium of the pyloric appendage of one species. The mid-gut epithelium contained cells reactive with antibodies to glucagon (three species), gastrin (five species), pancreatic polypeptide (five species), and substance P (two species). Cells immunoreactive for met-enkephalin were found in the epithelium of both the mid-gut and the stomach of six species. In six species in which the endocrine pancreas was investigated, insulin-, glucagon-, and
somatostatin
-like immunoreactivity was observed. Pancreatic polypeptide was definitely localised by immunostaining in cells of the endocrine pancreas of only one out of three species examined. Vasocative intestinal polypeptide-, neurotensin-,
bombesin
-, and enkephalin-like immunoreactivity was identified in the gastrointestinal nerve fibres in various species. In view of the considerable species variation found, caution should be exercised in generalising about the peptides present in the gastrointestinal tract of fish.
...
PMID:Peptide hormone-like immunoreactivity in the gastrointestinal tract and endocrine pancreas of eleven teleost species. 38 3
Synthetic
bombesin
, perfused in the isolated canine pancreas at a rate of 340-380 ng/min for 10 min, elicited a 4-fold rise in insulin to a peak at 2 min; a rapid decline followed discontinuation of
bombesin
. Glucagon rose by 50% to a peak at 6 min, but remained elevated after discontinuation of the
bombesin
.
Somatostatin
-like immunoreactivity was not significantly affected by perfusion with
bombesin
.
...
PMID:Bombesin stimulates the release of insulin and glucagon, but not pancreatic somatostatin, from the isolated perfused dog pancreas. 38 99
Somatostatin
(SRIF) has been tested for its actions on the central nervous system to affect glucoregulation. In doses ineffective when given systemically , SRIF and SRIF analogs given intracisternally (ic) reduce hyperglycemia and hyperglucagonemia after ic
bombesin
administration. The SRIF analog, des-AA1, 2, 4, 5, 12, 13-[D-Trp8]SRIF, decreases plasma insulin and elevates plasma glucose and glucagon when given systemically. However, when given ic, this peptide prevents the rise in glucose and glucagon after ic
bombesin
administration and is 10 times more potent than SRIF in reducing
bombesin
-induced hyperglycemia. Other analogs of SRIF and various unrelated peptides were found to be ineffective in reducing
bombesin
-induced hyperglycemia. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF prevented the hyperglycemia induced by surgical stress or by ic administration of beta-endorphin or carbacol. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF given ic did not prevent hyperglycemia induced by systemic administration of epinephrine, arginine, or glucagon. These studies suggest that SRIF and its analogs may act within the brain to affect glucoregulation.
...
PMID:Somatostatin: central nervous system actions on glucoregulation. 44 91
Bombesin acts within the brain to produce a prompt and sustained hyperglycemia, hyperglucagonemia, and relative or absolute hypoinsulinemia. Bombesin does not decrease plasma glucose turnover. Acute adrenalectomy but not hypophysectomy prevents hyperglycemia and hyperglucagonemia after intracisternal administration of
bombesin
. Administration of
bombesin
into the lateral ventricle of awake, unrestrained animals results in elevation of plasma glucose, preceded by a significant increase in plasma epinephrine and no increase in plasma norepinephrine or dopamine. Systemic administration of
somatostatin
prevents
bombesin
-induced hyperglycemia and hyperglucagonemia. These data support the conclusion that
bombesin
acts within the brain to increase sympathetic outflow resulting in increased adrenalmedullary epinephrine secretion, followed by depression of plasma insulin and elevation of plasma glucagon and glucose.
...
PMID:Central nervous system action of bombesin: mechanism to induce hyperglycemia. 46 25
In studies in dogs the gastrin response to food, to
bombesin
(1 micrgoram/kg-hr), and to
somatostatin
(2.5 and 5.0 microgram/kh-hr) plus food before and after truncal vagotomy was determined. Vagotomy caused an increase in basal levels of gastrin and in the release of gastrin after
bombesin
and food. Vagotomy augmented
somatostatin
suppression of food-stimulated gastrin release in a dose-dependent manner. We suggest that vagotomy causes a loss of both stimulatory and inhibitory vagal effects on gastrin release. Loss of vagal inhibition results in increased gastrin release to
bombesin
and food. Loss of vagal stimulation results in intensification of
somatostatin
-induced inhibition of postprandial gastrin release.
...
PMID:Influence of vagus on mechanisms for stimulation and inhibition of gastrin release. 64 65
Pulmonary neuroepithelial endocrine cells have been shown to contain serotonin-immunoreactivity in almost every species studied. Regulatory peptides, of which at least ten have been reported so far, were mostly only demonstrated in a number of the investigated species or in a subpopulation of neuroepithelial endocrine cells. Calcitonin gene-related peptide, calcitonin,
bombesin
/gastrin-releasing peptide, enkephalin,
somatostatin
, substance P, cholecystokinin and polypeptide YY were found in normal lung tissues, whereas ACTH and several other bioactive substances should be regarded as ectopic. The human pulmonary neuroepithelial endocrine system seems to harbour the largest spectrum of bioactive mediators. The distribution patterns of bioactive substances in various subpopulations of solitary neuroepithelial endocrine cells or neuroepithelial bodies and in different cells of a single neuroepithelial body reveal a great complexity. Therefore, further research is needed to elucidate the chemical coding of this system.
...
PMID:Comparative histological overview of the chemical coding of the pulmonary neuroepithelial endocrine system in health and disease. 128 Sep 75
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