Protein synthesis inhibitors attenuate water flow in vasopressin-stimulated toad urinary bladder

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...

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Bibliographic Details
Published in:	The American journal of physiology Vol. 254; no. 1 Pt 2; pp. F139 - F144
Main Authors:	Hoch, B S, Ast, M B, Fusco, M J, Jacoby, M, Levine, S D
Format:	Journal Article
Language:	English
Published:	United States 01-01-1988
Subjects:	1-Methyl-3-isobutylxanthine - pharmacology 550201 - Biochemistry- Tracer Techniques 8-Bromo Cyclic Adenosine Monophosphate - pharmacology AMIDES AMP AMPHIBIANS ANIMALS ANTI-INFECTIVE AGENTS ANTIBIOTICS ANTINEOPLASTIC DRUGS AQUATIC ORGANISMS BASIC BIOLOGICAL SCIENCES BIOCHEMISTRY BIOLOGICAL EFFECTS BIOLOGICAL MATERIALS BIOLOGICAL WASTES BLADDER BODY BODY FLUIDS Bufo marinus CARBON 14 COMPOUNDS CARBONIC ACID DERIVATIVES CHEMISTRY CYCLOHEXIMIDE Cycloheximide - pharmacology DRUGS ENZYMES FUNGICIDES HORMONES LABELLED COMPOUNDS MATERIALS NUCLEOTIDES ORGANIC COMPOUNDS ORGANIC NITROGEN COMPOUNDS ORGANS PEPTIDE HORMONES PERMEABILITY PESTICIDES PHOSPHORUS-GROUP TRANSFERASES PHOSPHOTRANSFERASES PHYSIOLOGY PITUITARY HORMONES Protein Kinases - metabolism Protein Synthesis Inhibitors - pharmacology PUROMYCIN Puromycin - pharmacology TOADS TRANSFERASES UPTAKE UREA Urinary Bladder - drug effects URINARY TRACT Urination - drug effects URINE VASOPRESSIN Vasopressins - pharmacology VERTEBRATES WASTES
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Summary:	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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0002-9513 2163-5773
DOI:	10.1152/ajprenal.1988.254.1.f139