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Chloride secretagogues stimulate inositol phosphate formation in shark rectal gland tubules cultured in suspension
Author(s) -
Ecay Tom W.,
Valentich John D.
Publication year - 1991
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041460311
Subject(s) - inositol phosphate , inositol , ionomycin , endocrinology , medicine , inositol trisphosphate , secretagogue , calcium , receptor , forskolin , inositol trisphosphate receptor , chemistry , phospholipase c , biology , vasoactive intestinal peptide , secretion , biochemistry , stimulation , neuropeptide
Neuroendocrine activation of transepithalial chloride secretion by shark rectal gland cells is associated with increases in cellular cAMP, cGMP, and free calcium concentrations. We report here on the effects of several chloride secretagogues on inositol phosphate formation in cultured rectal gland tubules. Vasoactive intestinal peptide (VIP), atriopeptin (AP), and ionomycin increase the total inositol phosphate levels of cultured tubules, as measured by ion exchange chromatography. Forskolin, a potent chloride secretagogue, has no effect on inositol phosphate formation. The uptake of 3 H‐myo‐inositol into phospholipids is very slow, preventing the detection of increased levels of inositol trisphosphate. However, significant increases in inositol monophosphate (IP 1 ) and inositol biphosphate (IP 2 ) were measured. The time course of VIP‐ and AP‐stimulated IP 1 and IP 2 formation is similar to the effects of these agents on the short‐circuit current responses of rectal gland monolayer cultures. In addition, aluminum fluoride, an artificial activator of guanine nucleotide‐binding proteins, stimulates IP 1 and IP 2 formation. We conclude that rectal gland cells contain VIP and AP receptors coupled to the activation of phospholipase C. Coupling may be mediated by G‐proteins. Receptor‐stimulated increases in inositol phospholipid metabolism is one mechanism leading to increased intracellular free calcium concentrations, an important regulatory event in the activation of transepithelial chloride secretion by shark rectal gland epithelial cells.