Cross-talk of phosphoinositide- and cyclic nucleotide-dependent signaling pathways in differentiating avian nasal gland cells.

In many bird species, the nasal glands secrete excess salt ingested with drinking water or food. In ducks ( Anas platyrhynchos), osmotic stress results in adaptive cell proliferation and differentiation in the gland. Using 'naive' nasal gland cells isolated from animals that had never ingested excess salt or 'differentiated' cells from animals fed with a 1% NaCl solution for 48 h, we investigated the allocation of metabolic energy to salt excretory processes and to other cellular activities. Activation of muscarinic acetylcholine receptors (carbachol) or beta-adrenergic receptors (isoproterenol) in nasal gland cells resulted in a transient peak in metabolic rate followed by an elevated plateau level that was maintained throughout the activation period. Activation of cells using vasoactive intestinal peptide, however, had only marginal effects on metabolic rate. In differentiated cells, sequential stimulation with carbachol and isoproterenol resulted in additive changes in metabolic rate during the plateau phase. Naive cells, however, developed supra-additive plateau levels in metabolic rates indicating cross-talk of both signaling pathways. Using bumetanide, TEA or barium ions to block different components of the ion transport machinery necessary for salt secretion, the relative proportion of energy needed for processes related to ion transport or other cellular processes was determined. While differentiated cells in the activated state allocated virtually all metabolic energy to processes related to salt secretion, naive cells reserved a significant amount of energy for other processes, possibly sustaining cellular signaling and regulating biosynthetic mechanisms related to adaptive growth and differentiation.