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)

The effects of a range of neuropeptides were investigated on the membrane potential of the Schwann cells of the giant nerve fibre of the tropical squid. Vasoactive intestinal peptide (VIP) produced a dose-dependent, long-lasting hyperpolarization of the Schwann-cell membrane potential. Among peptides structurally related to VIP, similar effects were produced by peptide histidine isoleucine (PHI) but not by secretin and glucagon. Substance P and somatostatin also hyperpolarized the Schwann-cell membrane potential but via receptor systems distinct from those activated by VIP. Methionine enkephalin ([Met]-enkephalin) blocked the actions of all the above peptides as well as the effects of DL-octopamine and carbachol. The actions of [Met]-enkephalin upon the VIP responses were antagonized by naloxone. VIP produces its effects on the Schwann-cell membrane potential via a receptor system that is independent from those described previously which mediate the effects of carbachol and DL-octopamine. However, VIP can potentiate the effects of the latter systems. The actions of VIP on the Schwann cell are unlikely to be mediated via changes in adenosine 3',5'-cyclic monophosphate (cyclic AMP) levels and are insensitive to changes in the level of extracellular calcium in the superfusate. The actions of VIP are, however, potentiated in the presence of low concentrations of lithium ions suggesting that the VIP receptor may mediate its effects by inducing the hydrolysis of polyphosphatidylinositols in the Schwann-cell membrane. Evidence is presented for the existence of an endogenous VIP-like component in the normal hyperpolarizing action of giant-axon activity on the membrane potential of the Schwann cell.
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PMID:Peptidergic modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre. 243 97

Enkephalins are naturally occurring peptides with powerful opiate-like effects which have recently been found in nerves of the pancreas. To assess the nature and extent of the influence that opiates exert on the endocrine pancreas, we examined the effects of MET-enkephalin (MEK), leu-enkephalin, morphine, and the opiate antagonist naloxone (NAL) as well as adrenergic and cholinergic blockade on the hormone release from the isolated perfused dog pancreas. It was found that MEK (1-100 nM) dose dependently inhibited somatostatin release and stimulated insulin secretion. The effects of MEK (100 nM) were modulated by the prevailing glucose concentration. Thus, more pronounced changes in D and B cell release were obtained at high (11 mM) rather than at low (1.3 mM) glucose. Ten micromolar of morphine inhibited somatostatin and stimulated insulin secretion, effects being antagonized by NAL (10 microM). NAL (10 microM) similarly counteracted the MEK (50 nM)-induced pertubations in islet hormone secretion. NAL (10 microM) per se did not affect somatostatin or insulin secretion at 8.3 mM glucose. Infusions of either 1 microM phentolamine, 1 microM propranolol, or 1 microM atropine did not significantly alter the amount of somatostatin or insulin secretion during the infusion of 50 nM MEK. In conclusion, the results are suggestive of enkephalins reaching the islets by neural pathways and directly modifying islet hormone secretion by directly interacting with opiate receptors on the islet cells.
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PMID:Enkephalins and the secretion of pancreatic somatostatin and insulin in the dog: studies in vitro. 613 3