Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a study of the effect of somatostatin (growth-hormone release-inhibiting hormone) on plasma-renin in healthy volunteers, plasma-renin activity was measured by radioimmunoassay after the intravenous administration of somatostatin and also during frusemide-induced hyperreninaemia. While somatostatin was being given, basal values of renin were unchanged. Injection of frusemide alone produced hyperreninaemia; but, under somatostatin, renin release was inhibited by 45%. The results indicate that somatostatin is a potent inhibitor of renin and exerts its effect independent of sodium excretion, which was unchanged under somatostatin. Conceivably, somatostatin plays an important role in the regulation of endogenous renin release.
 ...
PMID:Inhibition of frusemide-induced hyperreninaemia by growth-hormone release-inhibiting hormone in man. 5 89

Immuno-cytochemical methods were used to identify, in light and electron microscopy, the somatostatin-containing cells of the human antral mucosa. By means of immunoperoxidase and immunofluorescence methods sequentially applied on the same section, it was shown that the somatostatin cells are distinct from the gastrin cell population; these two endocrine cell types are often closely related. On ultrathin sections from aldehyde-fixed. Epon-araldite embedded tissues, the site of storage of somatostatin was localized with the peroxidaseantiperoxidase complexes technique, after removal of the resin by means of sodium ethoxide. This procedure represents a new technical approach to the use of electron-cytochemical techniques. The results indicate that somatostatin, a growth hormone release inhibiting factor, is localized in the endocrine granules of the D cells.
 ...
PMID:Immuno-electron-cytochemical localization of the somatostatin cells in the human antral mucosa. 7 94

The effect os somatostatin (SS) and of its analogs D Trp 8-SS and Asn 5-SS was studied upon the external pancreatic secretion of the Rat after stimulation by 2 deoxy-D-glucose. The secretion of sodium and bicarbonate was similarly inhibited by all four peptides. The analog D Trp 8-SS was more effective in inhibiting pancreatic protein excretion.
 ...
PMID:[Action of somatostatin and 3 analogs on external pancreatic secretion in the rat]. 10 39

Shifts in the distribution of the monovalent cations Na+ and K+ between the extra- and intracellular space seem to be important for the secretory response of the beta-cell. An attempt was therefore made to study the enzyme responsible for monovalent cation transport, the (NaK)-activated ATPase. In the presence of NaN3 as inhibitor of the mitochondrial Mg-ATPase, a NaK-ATPase with a specific activity of 72 mU X mg protein-1 could be demonstrated in crude membrane preparations of rat pancreatic islets. The enzyme, which was inactive in the absence of Mg++, needed both Na+ and K+ for activation and was inhibited by ouabain and PCMB. The main part of the NaK-ATPase was localized in the microsomal fraction. Glucose, sulphonylureas, somatostatin and diazoxide were without effect on NaK-ATPase.
 ...
PMID:NaK-ATPase in rat pancreatic islets. 14 87

In order to understand the mechanism by which cyclic 3':5'-adenosine monophosphate (cAMP) regulates insulin secretion, cAMP-dependent protein phosphorylation was studied in a transplantable hamster islet cell tumor. Single cell suspensions prepared by enzymatic digestion of the tumors released insulin into the incubation media. Glucagon (3 nM to 3 muM) stimulated cellular cAMP accumulation and insulin release in a dose-dependent manner and these effects were enhanced by 1 mM theophylline. 8-Bromoadenosine 3':5'-monophosphate (8Br-cAMP) (1 mM) increased insulin release. Somatostatin (10 mug/ml) inhibited basal and glucagon or 8Br-cAMP-stimulated insulin release without significantly lowering cellular cAMP in glucagon-stimulated cells. For analysis of phosphoproteins, cells were incubated with carrier-free 32Pi following which lysates were prepared and analyzed by sodium dodecyl sulfate slab gel electrophoresis and autoradiography. Of the numerous 32P-labeled protein bands found, only one (P1, Mr = 28,000) displayed a significant increase in 32P incorporation when cells were incubated under conditions that raise the concentration of cellular cAMP. Somatostatin did not affect 32P incorporation into P1 or any other protein band. When cells were incubated with glucagon, an increase in cellular cAMP was evident after 1 min, enhanced 32P incorporation into P1 after 1 to 5 min, and stimulation of insulin release after 5 to 10 min. Analysis of subcellular fractions led to the designation of P1 as a 40 S ribosomal protein. Two-dimensional electrophoresis of 32P-labeled basic ribosomal proteins showed two labeled proteins, P1 and P2, both of which were localized to the 40 S ribosomal subunit. Only phosphorylation of P1 was stimulated by cAMP. The cAMP-dependent ribosomal phosphoprotein, P1, may be identical with a ribosomal phosphoprotein demonstrated in a variety of tissues and species. Its physiological role remains to be established.
 ...
PMID:Cyclic adenosine 3':5'-monophosphate-mediated insulin secretion and ribosomal protein phosphorylation in a hamster islet cell tumor. 18 14

The action of somatostatin on compostition and flow rate of pure pancreatic juice obtained by endoscopic cannulation of the main pancreatic duct was evaluated in 5 healthy volunteers. Synthetic secretin (0.06 CU/kg-h) was intravenously infused throughout the 80-min study. Bicarbonate concentrations in pancreatic juice achieved constant levels (117 +/- 3 muEq/ml) after 10 min, whereas a steady state of juice flow (7.3 +/- 1.4 ml/5 min) was attained after 15 min of secretin infusion. In the third 20-min period, cyclic somatostatic (5 mug/kg-h i.v.) was given, leading to a decrease in pancreatic flow rate by 47% after 10 min, and by 67% after 15 min of somatostatin administration. Alrady 5 min after the infusion of somatostatin had been discontinued, pancreatic flow rate gradually recovered; presomatostatin levels, however, were not reached within 20 min. Cyclic AMP varied roughly in accordance with bicarbonate concentrations, whereas the chloride concentrations were reciprocally related. Bicarbonate, sodium, potassium, protein, and cyclic GMP concentrations did not change substantially due to somatostatin.
 ...
PMID:Inhibition by somatostatin of secretin-stimulated pancreatic secretion in man: a study with pure pancreatic juice. 18 82

Two somatostatin analogues (SA) and 17-alpha-dihydroequilin (E) inhibited the stereospecific binding of 3H-naloxone in vitro to rat brain opiate receptors in the absence of sodium. The addition of sodium indicated the SA to be greater or similar in potency to somatostatin as opiate agonists and E to be an opiate antagonist. The results indicate that SA and certain steroids may affect endorphin containing neurons.
 ...
PMID:Effect of somatostatin analogues and 17-alpha-dihydroequilin on rat brain opiate receptors. 21 Apr 85

Two minutes after the intravenous administration of 1 ml of sheep somatostatin antiserum in the rat, plasma growth hormone (GH) levels had reached a maximal 10-15-fold increase which remained approximately constant up to 90 min. The injection of sodium pentobarbital (2 mg/100 g body wt) led to a rapid and transient rise of plasma GH levels of similar magnitude (10-fold) reached 20 to 40 min after injection of the narcotic. The important finding is, however, that the combined administration of somatostatin antiserum and pentobarbital or morphine led to an almost exact additive effect on the plasma GH concentrations. These data, beside providing additional evidence for the existence of GH-releasing activity (GH-RH), indicate that morphine and pentobarbital stimulate GH secretion through increased release of GH-RH.
 ...
PMID:Stimulated release of hypothalamic growth hormone-releasing activity by morphine and pentobarbital. 32 63

An attempt is made in this review to elucidate the functional characteristics of paraneurons. The secretory functions of neuron, neurosecretory cell and paraneuron consist of three main phases: secretion, transmission and reversion. Secretion can be divided into a steady state and an activated state. A paraneuron behaves characteristically in the active phase of secretion and in the phase of transmission. There are three main events in the activated phase of secretion ("stimulus-extrusion coupling") in paraneurons, reception of stimulus, conduction of excitation, and extrusion of secretory substances. These three events seem to correspond to the functional characteristics in the three different regions of the paraneuron membrane. A stimulus-induced change in conformation in the input region of paraneurons may result in the inward movement of Na+ and Ca++. The inward movement of Na+ sometimes coincides with a graded depolarization which may occasionally generate all-or-nothing, short-duration action potential possibly in the intermediate region. A rise in [Ca++]i, whether it coincides with Na-dependent depolarization or not, may initiate extrusion of granules. If eccytosis is the mode of extrusion of secretory granules of paraneurons, the cell membranes at the output region should be rearranged by fusion with the membranes of granules. Ionic permeability of the output region might decrease during eccytosis if ionic permeability of the granule membrane is lower than that of other regions. Somatostatin in most cases and insulin in a special case may act locally on the adjacent target cells, and such a mode of transmission may come into the category of paracrine secretion.
 ...
PMID:Physiology of paraneurons. 35 76

Intravenous infusion of somatostatin in mongrel dogs caused a significant decrease in the peripheral plasma renin activity (PRA) enhanced by pentobarbital sodium anesthesia or furosemide treatment. However, the inhibitory activity vanished within 10 min after termination of somatostatin infusion. Intrarenal arterial infusion of somatostatin decreased furosemide-enhanced PRA in renal vein by 24.0%, 16.6% and 8.6% in dose of 0.1, 0.5 and 1.0 microgram, respectively. On the other hand, high doses of the peptide (50-200 microgram) failed to decrease. The changes in PRA occurred in the absence of any alteration in blood pressure during the intravenous infusion under furosemide treatment. In an in vitro study, the addition of somatostatin in doses of 0.01 and 0.05 microgram suppressed the renin release in dog renal cortical cell suspension by 74.3% and 53.6%, respectively. Therefore, in both intrarenal arterial infusion and the cell suspension system, somatostatin was increasingly effective in decreasing renin release towards the lower end of the dose range tested. These results suggest that the effect of somatostatin on hyperreninemia may involve an inhibition of renin release at the cell level in the kidney.
 ...
PMID:Effect of somatostatin on plasma renin activity. 47 26


1 2 3 4 5 6 7 8 9 10 Next >>