Hypertonic sucrose treatment enhances second messenger accumulation in vasopressin-sensitive cells

Ward Lutz, Rajiv Kumar

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16 Citations (Scopus)

Abstract

When we treated vasopressin sensitive vascular smooth muscle cells (A10 cells) and kidney cells (LLC-PK1 cells) with hypertonic sucrose and vasopressin, we observed a decrease in the internalization of radiolabeled vasopressin into these cells and an increase in the amount of second messenger present in these cells following vasopressin stimulation. In A10 cells exposed to hypertonic sucrose, there was an increase in the amount of cellular inositol phosphates accumulated in response to vasopressin compared with cells not exposed to hypertonic sucrose. Similarly, in hypertonic sucrosetreated LLC-PK1 cells, vasopressin increased the amount of adenosine 3′,5′-cyclic monophosphate (cAMP) present within the cells compared with LLC-PK1 cells not exposed to hypertonic sucrose. Hypertonic sucrose treatment inhibited receptor-mediated endocytosis in both these cell lines. Hypertonic sucrose alone did not increase the basal amounts of inositol phosphates or cAMP present in A10 or LLC-PK1 cells, respectively. Hypertonic sucrose treatment inhibits receptor endocytosis and increases second messenger concentrations in vasopressin-sensitive cells.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume264
Issue number2 33-2
StatePublished - 1993

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Second Messenger Systems
Vasopressins
Sucrose
LLC-PK1 Cells
antineoplaston A10
Inositol Phosphates
Endocytosis
Vascular Smooth Muscle
Adenosine
Smooth Muscle Myocytes
Kidney
Cell Line

Keywords

  • Receptor-mediated endocytosis

ASJC Scopus subject areas

  • Physiology

Cite this

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abstract = "When we treated vasopressin sensitive vascular smooth muscle cells (A10 cells) and kidney cells (LLC-PK1 cells) with hypertonic sucrose and vasopressin, we observed a decrease in the internalization of radiolabeled vasopressin into these cells and an increase in the amount of second messenger present in these cells following vasopressin stimulation. In A10 cells exposed to hypertonic sucrose, there was an increase in the amount of cellular inositol phosphates accumulated in response to vasopressin compared with cells not exposed to hypertonic sucrose. Similarly, in hypertonic sucrosetreated LLC-PK1 cells, vasopressin increased the amount of adenosine 3′,5′-cyclic monophosphate (cAMP) present within the cells compared with LLC-PK1 cells not exposed to hypertonic sucrose. Hypertonic sucrose treatment inhibited receptor-mediated endocytosis in both these cell lines. Hypertonic sucrose alone did not increase the basal amounts of inositol phosphates or cAMP present in A10 or LLC-PK1 cells, respectively. Hypertonic sucrose treatment inhibits receptor endocytosis and increases second messenger concentrations in vasopressin-sensitive cells.",
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