Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Continuous injection of L-pyroglutamate (L-PGA) into the rat striatum induces a lesion with three regions: a necrotic core, a rim of pyknotic cells, and a peripheral spongiose region. The L-PGA was administered through an implanted intrastriatal cannula coupled to an Alzet osmotic pump loaded with one of three doses of L-PGA (3, 5, or 13 times the normal amount of L-PGA/g wet wt rat forebrain (23 nmol/g). The magnitude of the lesion was dependent upon the concentration of buffered L-PGA and the duration of continuous pumping. The necrotic region contained macrophages and neutrophils, while condensed neurons and oligodendroglial cells were present in the pyknotic region. The spongiose region contained vacuolated neuropil and degenerating nerve cells and oligodendroglia. The spongiose region blends with the normal neuropil. A population of aspiny neurons were identified throughout the spongiose region. These neurons stained positive for NADPH diaphorase and demonstrated a somatostatin-like immunoreactivity similar to that of the aspiny neurons spared in Huntington's disease and in the neurotoxin-induced striatal-lesioned rat models of Huntington's disease.
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PMID:Chronic intrastriatal L-pyroglutamate: neuropathology and neuron sparing like Huntington's disease. 256 47

The effects of antramine, an antral histamine (AH), and of synthetic histamine (SH) on acid, pepsin, and gastrin responses to meals alone or in combination with somatostatin were studied in dogs equipped with a Heidenhain pouch. Food-induced acid secretion was potentiated by AH and only slightly increased by SH. Pepsin secretion was increased by AH and decreased by SH. Both AH and SH suppressed the inhibitory activity of somatostatin on food-induced secretion. AH potentiated gastrin response to feeding but decreased it when somatostatin was added to the meal. Since acid secretion was unrelated to gastrin response, it would appear that the secretory effects of AH involve a direct action on secreting cells, itself based on the suppression of somatostatin inhibition. Gastric secretion is probably related to gastrin efficacy on secreting cells, which would result from the antagonistic effects of somatostatin and AH. These data suggest an alternative hypothesis concerning the role of histamine in the control of gastric secretion.
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PMID:Antramine (antral histamine) antagonizes somatostatin inhibition on endogenous gastrin-induced gastric secretion. A new hypothesis for the role of histamine in gastric secretion regulation. 286 68

In vivo secretion of gastric acid and pepsin has been studied in pylorus-ligated cod. Basal acid output amounted to 100-150 mumol H+.kg-1.h-1 and pepsin secretion to 1 mg.kg-1.h-1. In response to bombesin nonapeptide (2.4 nmol.kg-1.h-1) and histamine (81 nmol.kg-1.h-1), acid secretion increased to approximately 200 and 600% of the basal level, respectively. Pepsin output was marginally affected by histamine but increased to approximately 3 and 15 times the basal level during treatment with bombesin and eledoisin (3.27 nmol.kg-1.h-1). Somatostatin (SS-14, 15 nmol.kg-1.h-1) inhibited basal acid secretion by 85%. It also inhibited the acid secretion during stimulation with bombesin (68%) and histamine (57%), but although the former effect could be explained by removal of the basal component, the latter could not. Basal pepsin secretion was not affected by SS-14. A slight inhibition (28%) of the peak pepsin response to eledoisin was demonstrated, and bombesin failed to stimulate pepsin secretion during treatment with SS-14. These results indicate that endogenous somatostatin, if present in the cod stomach, could play a role in the regulation of gastric secretion.
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PMID:Effect of somatostatin on basal and stimulated gastric secretion in the cod, Gadus morhua. 289 72

The gastric acid and pepsin inhibitory activities of 21 analogues of somatostatin, the majority modified at position 8, were determined in conscious cats in order to examine the importance of Trp8 for the activity of somatostatin. Pepsin secretion stimulated by pentagastrin was 5 times more sensitive, compared with the acid secretion, to inhibition by somatostatin. All the analogues showed similar differential sensitivity, indicating a similar specificity of somatostatin receptors involved in the inhibition of these two secretions. Halogenated-Trp8 analogues of somatostatin were only equipotent or slightly more active than somatostatin against gastric secretion in the cat, whilst these analogues are up to 30 times more potent against growth hormone release in the rat, indicating a different specificity of the two groups of receptors. Studies with the position 8 modified analogues suggest that the electron density of the aromatic nucleus of Trp8 may be relatively unimportant in determining the gastric inhibitory activity, whilst it can be concluded that the role of Trp8 in somatostatin depends to a large extent on the indole NH group. The precise role of Trp8 in somatostatin could be an involvement in the binding of somatostatin to its receptors, or involvement in forming the biologically active conformation of somatostatin.
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PMID:Structure-activity studies with somatostatin: the role of tryptophan in position 8. 611 15

1. The effect of i.v. administration of prostaglandin (PG) E(2) (10-40 mug kg(-1) h(-1)), 16,16-dimethyl PGE(2) (0.1-0.5 mug kg(-1) h(-1)), PGE(1) (16-20 mug kg(-1) h(-1)), PGA(1) (5-11 mug kg(-1) h(-1)) and PGF(2alpha) (40 mug kg(-1) h(-1)) on the relationship between [H(+)] and flow of gastric juice during stimulation of gastric secretion by pentagastrin was investigated in conscious cats prepared with cannulated gastric fistulae.2. A- and E-type prostaglandins significantly reduced pentagastrin-stimulated acid output. This inhibition was associated with a reduction of the [H(+)] of the gastric juice such that the [H(+)] observed at any flow rate tended to be lower than the normal range observed with pentagastrin alone. With the highest doses of these prostaglandins the mean [H(+)] values were well below the normal range with pentagastrin alone.3. At the dose tested, PGF(2alpha) had little effect on acid output, and did not alter the relationship between [H(+)] and gastric flow.4. There is a linear relationship between acid output and gastric flow and this relationship is similar during stimulation of gastric secretion by pentagastrin, histamine or insulin. Gastric acid inhibitory doses of cimetidine, atropine and somatostatin did not alter this relationship. In contrast the A- and E-type prostaglandins displaced this relationship to the right of the normal line observed with the acid stimulants alone. A- and E-type prostaglandins reduced the slope of the line relating acid output and gastric flow from approximately 150-170 muequiv/ml(-1) to approximately 100-120 muequiv ml(-1), this being taken as evidence of dilution of the parietal H(+) secretion with a non-parietal secretion.5. The volume of non-parietal gastric secretion was calculated as the gastric flow at zero acid output by extrapolation of linear plots of acid output versus gastric flow. Unstimulated gastric flow measured directly was 0.75 ml 15 min(-1). The calculated non-parietal flow was in the range 0.52-0.90 ml 15 min(-1) during stimulation of gastric secretion with pentagastrin, histamine and insulin, and inhibition of pentagastrin-stimulated acid secretion with cimetidine, atropine and somatostatin. PGE(2) (1.51 ml 15 min(-1)) and 16,16-dimethyl PGE(2) (1.20 ml 15 min(-1)) nearly doubled the calculated non-parietal flow.6. These data demonstrate that gastric acid inhibitory doses of A- and E-type prostaglandins can reduce the [H(+)] in the bulk fluid of the gastric lumen during stimulation of acid secretion. The data provide evidence that these prostaglandins stimulate a non-parietal component of gastric secretion. This might be gastric bicarbonate and mucus secretion.
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PMID:Prostaglandins alter the relationship between gastric hydrogen ion concentration and flow: evidence for stimulation of non-parietal secretion in the cat. 694 8