Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cultured retinal glial cells from the rat are responsive to modulation by vasoactive intestinal peptide (VIP). VIP (1 X 10(-6) M) elevated the intracellular cyclic AMP concentration from the basal level of (4.4-11.1) p mole/mg protein to (354-440) p mole/mg protein in three minutes at 25 degrees C. The half-maximal concentration is 4.8 X 10(-8) M, which is similar to that observed in the cultured retinal glial cells from the chick embryo.
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PMID:VIP modulation of cultured glial cells of the rat retina. 255 50

1. The effects of autonomic stimulation on the release of vasoactive intestinal peptide (VIP) from the gastrointestinal tract have been investigated in adrenalectomized claves 2-5 weeks after birth.2. Stimulation of the peripheral ends of the splanchnic nerves (10 Hz for 10 min) caused a small fall in the concentration of VIP in portal and arterial plasma, together with a rise in the concentration in intestinal lymph. None of these changes achieved statistical significance.3. The effects of stimulation of the peripheral ends of the thoracic vagi, below the heart (10 Hz for 10 min), were found to depend in part upon the integrity of the splanchnic sympathetic innervation. A substantial rise in the concentration of VIP in intestinal lymph occurred whether or not the splanchnic nerves had been cut whereas an associated rise in arterial plasma VIP was only observed in calves in which the splanchnic nerves had been sectioned.4. The rise in the concentration of VIP in intestinal lymph, in response to vagal stimulation, was unaffected by concomitant stimulation of the splanchnic nerves, although the associated rise in arterial plasma VIP concentrations was suppressed. The response was also found to be resistant to atropine.5. The minimum estimated concentration of VIP in the extracellular fluid of the gastrointestinal tract was estimated to be about 60 p-mole/l. at rest and to rise by 70-120 p-mole/l. in response to vagal stimulation.6. Intravenous infusions of VIP at a dose of 50 ng kg(-1) min(-1) (16 p-mole kg(-1) min(-1)), which raised the minimum estimated concentration of VIP in the gastro-intestinal tract to the highest range encountered during stimulation, produced no significant changes in the concentrations of glucose, insulin, pancreatic glucagon or pancreatic polypeptide in the arterial plasma.7. It is concluded that a small amount of VIP is released from the gastrointestinal tract in response to vagal stimulation. In contrast, release of VIP is unaffected by stimulation of the splanchnic nerves except in so far as the rate at which the peptide passes into the circulation is reduced by adrenergic vasoconstriction.
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PMID:Effects of autonomic stimulation on the release of vasoactive intestinal peptide from the gastrointestinal tract in the calf. 699 67

Using an in vitro incubation system, the role of the cyclic AMP-dependent protein kinase A (PKA) pathway in the regulation of the in situ activity of tyrosine hydroxylase (TH) was studied in the hypothalamuses of young and aged ovariectomized rats. Hypothalamic tissue was incubated for 60 min in medium containing 3-hydroxybenzylhydrazine dihydrochloride, a dihydroxyphenylalanine (DOPA) decarboxylase inhibitor, and various agents that modify the activity of the PKA pathway. At the end of the incubation, the tissue was homogenized and analyzed for DOPA and TH mass. The in situ molar activity of TH was expressed as the moles of DOPA accumulating in the tissue per mole of TH per hour. Forskolin, an activator of adenylyl cyclase and the cyclic AMP agonist, (Sp)-cyclic adenosine 3',5'-monophosphothioate, significantly (P < .01) increased the in situ molar activity of TH in the hypothalamic dopaminergic (DAergic) neurons of both young and aged rats. Theophylline, a phosphodiesterase inhibitor, did not affect the TH molar activity in the hypothalamuses of aged animals but did significantly (P < .001) increase its activity in those of young rats. When vasoactive intestinal peptide was evaluated, the TH molar activity was significantly (P < .005) increased in the hypothalamuses of young rats but not in those of aged rats. It was suggested that the deficiency of DA secretion by hypothalamic DAergic neurons of aged rats may be the result of insufficient activation of PKA caused by failure of transduction of an extracellular signal to activate adenylyl cyclase and produce cyclic AMP.
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PMID:Localization of a defect in hypothalamic dopaminergic neurons of the aged brain that results in impaired PKA-dependent activation of tyrosine hydroxylase. 790 91

The purpose of this study was to determine whether encapsulation of vasoactive intestinal peptide (VIP) in liposomes enhances its vasoactive effects. Liposomes were formed from a solution of VIP in phospholipids and cholesterol, resulting in incorporation of 0.008 mole peptide/mole phospholipid. Leakage of VIP from the liposomes was undetectable over several days of incubation at 4 degrees C in 0.15 M sodium chloride. Under conditions permitting rapid hydrolysis of VIP by trypsin, there was no breakdown of the encapsulated peptide. Increasing concentrations of the liposome-encapsulated VIP administered intravenously to anesthetized hamsters produced a concentration-dependent decrease in the mean arterial blood pressure. The duration and magnitude of the hypotensive effect of the encapsulated VIP was significantly greater (p < 0.05) compared to equivalent concentrations of the unencapsulated peptide. Infusion of empty liposomes was without significant effect on the mean arterial blood pressure. We conclude that encapsulation of VIP in liposomes potentiates the blood pressure-lowering effect of the peptide.
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PMID:Vasoactive intestinal peptide encapsulated in liposomes: effects on systemic arterial blood pressure. 815 24