Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.4.1 (phosphodiesterase)
18,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was performed to examine the effects of somatostatin on antral gastrin release stimulated by postreceptor increases in adenosine cyclic nucleotide. Increases in intracellular levels of cyclic adenosine monophosphate were achieved through the use of the dibutyryl derivative of cyclic adenosine monophosphate and the phosphodiesterase inhibitor theophylline. The effects of somatostatin on basal and stimulated gastrin release were examined in rat antral organ culture experiments. Inclusion of somatostatin in the culture medium (1 X 10(-8) to 1 X 10(-4) M) resulted in significant inhibition of gastrin release at somatostatin concentrations of 1 X 10(-5) and 1 X 10(-4) M: both doses of somatostatin inhibited gastrin release by approximately 52% at 30 min and by 32% at 6 h. Gastrin release stimulated by dibutyryl cyclic adenosine monophosphate was significantly inhibited by 1 X 10(-5) and 1 X 10(-4) M somatostatin to 133% and 121% at 30 min and 77% and 98% at 6 h, respectively. Gastrin release stimulated by theophylline (1 mM) was also significantly inhibited by somatostatin in doses ranging from 1 X 10(-6) to 1 X 10(-4) M. The degree of inhibition by somatostatin of dibutyryl cyclic adenosine monophosphate- and theophylline-stimulated gastrin release declined over the duration of culture. In conclusion, these results suggest that somatostatin inhibits adenosine cyclic nucleotide-stimulated gastrin release by acting at a point distal to the formation of cyclic adenosine monophosphate.
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PMID:Postreceptor inhibition of antral gastrin release by somatostatin. 285 45

The rectal gland of the spiny dogfish Squalus acanthias is stimulated to secrete chloride by vasoactive intestinal peptide (VIP) in a way that is inhibited by somatostatin. The mechanism of inhibition by somatostatin was studied in isolated perfused rectal glands and separated rectal gland cells. Somatostatin did not alter the specific binding of VIP to rectal gland cells but inhibited their accumulation of adenosine 3',5'-cyclic monophosphate (cAMP) in response to VIP. In isolated perfused glands, somatostatin inhibited the stimulation of secretion produced by VIP, adenosine, and forskolin, as well as by dibutyryl cAMP plus a phosphodiesterase inhibitor. The results support the hypothesis of both a proximal and a distal locus, in the cascade of events leading from adenylate cyclase activation to cellular response, at which somatostatin exerts an inhibitory effect.
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PMID:Mode of action of somatostatin to inhibit secretion by shark rectal gland. 286 85

The effects of pretreatment with pancreatic secretagogues and subsequently activated cellular events on [125I-Tyr1] somatostatin binding to acinar membranes were studied. Pretreatment of pancreatic acini with bombesin at increasing concentrations for 120 min reduced labeled somatostatin binding to the acinar membranes in a dose-dependent fashion with a maximal reduction of binding at 10(-8)M bombesin (44.3 +/- 1.8% of control). The maximal inhibition of labeled somatostatin binding by pretreatment with bombesin was almost comparable to that with COOH-terminal octapeptide cholecystokinin (CCK8) or carbamylcholine (carbachol). Furthermore, pretreatment of acini with vasoactive intestinal peptide (VIP) as well as secretin resulted in a small, but significant decrease of subsequent labeled somatostatin binding. In addition, adenosine 3', 5' cyclic nucleotide derivatives or a phosphodiesterase inhibitor mimicked the effect of VIP or secretin. The effect of simultaneous pretreatment of acini with VIP and carbachol on subsequent labeled somatostatin binding appeared to be almost equal to the calculated additive value for each peptide. These results suggest that the binding of somatostatin to its receptors in the pancreatic acini may be regulated via two functionally distinct pathways.
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PMID:[Effects of various pancreatic secretagogues on somatostatin binding to rat pancreatic acinar cell plasma membranes]. 288 Jul 53

The effect of somatostatin on the stimulation of adenosine-3',5'-cyclic monophosphate (cAMP) production by arginine vasopressin (AVP) was examined in rat renal papillary collecting tubule cells in culture. The presence of phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine AVP at a concentration of 1 X 10(-10) M or higher significantly increased cellular cAMP levels in a dose-dependent manner. The stimulation by AVP of cellular cAMP production was significantly attenuated by 1 X 10(-6) M somatostatin (1 X 10(-9) M AVP, 477.5 +/- 23.0 vs. 292.4 +/- 28.5 fmol/micrograms protein per 10 min, P less than 0.01). When the cells were pretreated with pertussis toxin, pertussis toxin completely abolished the inhibitory effect of somatostatin on cellular cAMP production in response to AVP. Such an effect was obtained with a concentration of 0.1 ng/ml or higher of pertussis toxin and an incubation time of longer than an hour. The exposure of cells to 100 ng/ml pertussis toxin for two hours recovered the cellular cAMP response to 1 X 10(-9) M AVP in the presence of 1 X 10(-6) M somatostatin, the value of which 527.1 +/- 32.6 fmol/micrograms protein per 10 minutes, was a comparable level to that in response to only 1 X 10(-9) M AVP. Also, somatostatin inhibited the cellular cAMP response to glucagon and cholera toxin, but did not inhibit basal and forskolin-stimulated cAMP levels. Pertussis toxin treatment of cells completely abolished these inhibitory effects of somatostatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversal of somatostatin inhibition of AVP-induced cAMP by pertussis toxin. 289 65

Pretreatment of pancreatic acini with vasoactive intestinal peptide (VIP) or secretin for 120 min reduced subsequent [125I-Tyr1]somatostatin binding to membranes prepared from these acini, with a maximally reduced binding being 79.2% or 77.4% of control, respectively. In addition, exogenously added cyclic AMP derivatives or a phosphodiesterase inhibitor mimicked the effect of VIP or secretin. Scatchard analysis of [125I-Tyr1]somatostatin binding demonstrated that the decrease in the labeled somatostatin binding induced by VIP or dibutyryl cyclic AMP (dbcAMP) pretreatment was due to the decrease in the maximum binding capacity without a significant change in the binding affinity. The effect of simultaneous pretreatment of acini with VIP and carbamylcholine (carbachol) on subsequent labeled somatostatin binding appeared to be almost equal to the calculated additive value for each peptide. Results obtained, therefore, indicate that the binding of somatostatin to its receptors in the pancreas may be regulated via two functionally distinct pathways.
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PMID:Pancreatic secretagogues regulate somatostatin binding to acinar cell membranes via two-functionally distinct pathways. 289 26

The chain of events leading to the manifestation of the biological action of somatostatin are described. Internalization is mediated by cytoskeletal proteins in the presence of calmodulin. Transduction of the somatostatin message at the membrane level takes place through inhibition of cyclic AMP accumulation and blockade of cytosol calcium increases. The influence of central and peripheral factors upon these processes is discussed and the importance of the Ni/Ns components is stressed. Thus, somatostatin also suppresses phosphoinositide turnover and stimulates soluble phosphodiesterase, thus reinforcing its negative effect on cyclase generation.
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PMID:Mechanism of action of somatostatin. 290 Jan 97

Somatostatin administration to female rats increased the activity of calmodulin-dependent soluble phosphodiesterase, both in pituitary and brain. This effect was also seen in homogenates of GH4C1 cells pretreated with the hormone. When assayed in the presence of EGTA no differences in rat brain and pituitary phosphodiesterase were observed between controls and somatostatin-treated, but when assayed in the presence of calcium or calcium plus calmodulin a clear increase in the activity of the enzyme was detected. In GH4C1 homogenates prepared from somatostatin-pretreated cells there was an increase in phosphodiesterase activity assayed in the presence of EGTA vs non-treated controls, which was more clear when assayed in the presence of calcium or calcium plus calmodulin. These observations suggest that somatostatin effects derive, at least in part, from increased cyclic nucleotide degradation.
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PMID:Somatostatin stimulates phosphodiesterase in rat anterior pituitary and brain, and GH4C1 cells. 290 90

We have studied the in vitro effect of VIP and histamine on ultrastructure of the parietal cells in isolated guinea pig fundic glands. The morphological changes induced by histamine in the parietal cells can be compared to those observed after histamine stimulation in vivo or in vitro on gastric mucosa preparations. In contrast, VIP incubation did not produce the ultrastructural changes related to gastric acid secretion, in resting parietal cells. Pretreatment of the glands by VIP resulted in a remarkable suppression of the histamine effect, since the parietal cells assumed an almost resting state. The data (1) indicate that the parietal cells in isolated gastric glands of the guinea pig retain in vitro the capacity to undergo the ultrastructural changes that are related to acid secretion in vivo after histamine or cAMP and (2) suggest that VIP is an inhibitor of histamine-induced gastric acid secretion in the guinea pig. It is proposed that VIP could act directly on the parietal cell via cAMP-phosphodiesterase activation, or indirectly via gastric somatostatin and/or prostaglandin secretions, inhibiting the H2 receptor-cAMP system of the parietal cell.
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PMID:VIP inhibits histamine-induced ultrastructural changes related to acid secretion by parietal cells. 608 30

Glucose stimulates somatostatin release from perifused pancreatic islets of diabetic rats 42-47 days after the induction of diabetes, and 48 h after withdrawal of insulin replacement therapy. The glucose effect is augmented by theophylline or glucagon. Basal somatostatin release and glucose-induced secretion are significantly higher in diabetic islets than in controls. It is suggested that glucose promotes somatostatin release by directly interacting with islet D cells but not via indirect pathways. Glucose-induced stimulation appears to be modulated by a D-cell adenylate cyclase/phosphodiesterase system. Reasons responsible for increased somatostatin secretion by diabetic islets include reduction in B-cell mass, suggesting that B cells may normally suppress the secretory activity of D cells.
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PMID:Increased somatostatin secretion from pancreatic islets of streptozotocin-diabetic rats in response to glucose. 611 May 94

In dispersed mucosal cells from guinea-pig stomach, somatostatin inhibited in a noncompetitive fashion (Ki, 2 x 10(-8) M) the increase in cellular cyclic AMP caused by histamine but not by prostaglandin E1 or phosphodiesterase inhibitors. Somatostatin also inhibited the increase in [14C]aminopyrine uptake caused by low concentrations of histamine probably by interfering with the synthesis of cellular cyclic AMP.
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PMID:Direct action of somatostatin on dispersed mucosal cells from guinea-pig stomach. 611 31


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