Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin stimulates the introduction of aggregated particles, which may represent pathways for water flow, into the luminal membrane of toad urinary bladder. It is not known whether water transport pathways are degraded on removal from membrane or whether they are recycled. We examined the effect of the protein synthesis inhibitors cycloheximide and puromycin using repeated 30-min cycles of vasopressin followed by washout of vasopressin, all in the presence of an osmotic gradient, a protocol that maximizes aggregate turnover. "High dose" cycloheximide (200 micrograms/ml) inhibited flow immediately. "Low dose" cycloheximide (1 microgram/ml) did not affect initial flow; however, flow was inhibited by the fourth restimulation. On further rechallenge, inhibition persisted but did not increase. In the absence of vasopressin, inhibition did not develop. Despite the inhibition of flow in vasopressin-treated tissues, the cAMP-dependent protein kinase ratio (-cAMP/+cAMP), an index of in vivo cAMP effect, was elevated in cycloheximide-treated tissues, suggesting modulation at a distal site in the stimulatory cascade. Cycloheximide inhibited flow when 10 microM forskolin or 0.2 mM 8-BrcAMP was substituted for vasopressin in the fourth period; however, MIX (4 mM)-stimulated flow was enhanced by 1 microgram/ml cycloheximide but inhibited by 200 micrograms/ml cycloheximide. [14C]urea permeability was not inhibited by cycloheximide. Puromycin (0.5 mM) also inhibited water flow by the fourth challenge with vasopressin. The data suggest that protein synthesis inhibitors attenuate flow at a site that is distal to cAMP-dependent protein kinase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protein synthesis inhibitors attenuate water flow in vasopressin-stimulated toad urinary bladder. 244 2

Rat kidney cortex slices were incubated for 30 min at 37 degrees C in unmodified Krebs-Henseleit buffer containing aldosterone, vasopressin, theophylline, ethacrynic acid, frusemide, spironolactone or ouabain. Tamm-Horsfall glycoprotein (THG) released into the media was measured by radioimmunoassay and at the end of each experiment the slices were homogenized and assayed for THG content. Incubation of kidney cortex slices in unmodified buffer resulted in a significant increase in the slice THG content when compared with pre-incubation levels. The increase was prevented by puromycin or cycloheximide. Incubation in ethacrynic acid (1 mmol/l) or frusemide (10 mmol/l) resulted in a significant increase in release of THG when compared with unmodified buffer. Puromycin or cycloheximide failed to prevent the increased release. THG release induced by ethacrynic acid or frusemide is probably the result of an aggregation-disaggregation reaction on the cell membrane. It is suggested that the action of the chloride inhibiting diuretics, ethacrynic acid and frusemide, is mediated in some way via THG.
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PMID:Tamm-Horsfall glycoprotein release from rat kidney cortex slices in vitro. 647 53

Exposure of isolated hepatocytes to glucagon for 45 min caused a 2.5-fold increase in the time (Ca2+ retention time) for which mitochondria subsequently isolated from the cells retained a load of exogenous Ca2+ before its spontaneous release. Half maximal effect of glucagon was observed at a concentration of 0.6 nM. An increase in the Ca2+ retention time was observed after 30 but not 15 min exposure of cells to the hormone. Incubation of hepatocytes with dexamethasone, epinephrine, vasopressin, dibutyryl cyclic AMP or 8-bromo cyclic GMP also induced an increase in mitochondrial Ca2+ retention time. The effect of glucagon was associated with an increase in cellular cyclic AMP and was inhibited by puromycin, cycloheximide and cordycepin, but not by actinomycin D or chloramphenicol. Puromycin caused only a small inhibition of the stimulation by glucagon of mitochondrial pyruvate carboxylation. It is concluded that the effects of glucagon on mitochondrial Ca2+ retention require nuclear DNA-directed protein synthesis and differ, in this respect, from the rapid-onset effects of the hormone on other mitochondrial properties, including pyruvate carboxylation.
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PMID:On the effect of glucagon on mitochondrial calcium retention in isolated hepatocytes. 650 Apr 86