Author:
Walsh-Reitz M. M.,Toback F. G.
Abstract
The hypothesis that arginine vasopressin could regulate kidney epithelial growth by its effect on Na+ transport was examined in cultures of cells from the BSC-1 line. Addition of vasopressin (75 pg/ml) or NaCl (25 mM) to the medium stimulated growth of confluent cultures but retarded growth of sparse cells in the presence of 0.5% calf serum. Thus the capacity of vasopressin or exogenous NaCl to regulate growth of BSC-1 cells was cell density dependent. Vasopressin stimulated growth of confluent cultures only in the narrow concentration range of 50-100 pg/ml (approximately 10(-10)M), whereas concentrations of 10 pg/ml and 125-1,000 pg/ml had no effect. In contrast, vasopressin at or above concentrations of 10 pg/ml raised cell Na+ content to its maximal value, which indicated that the hormone could increase the Na+ content of cells without necessarily stimulating their growth. To determine if vasopressin modulates growth by acting on the plasma membrane, nutrient transport and ligand binding were assessed in high-density quiescent cultures. The hormone augmented uptake of alpha-aminoisobutyric acid and binding of epidermal growth factor, whereas the addition of NaCl (25 mM) did not. Thus growth stimulation by vasopressin was associated with increased cell Na+ content, enhanced uptake of an amino acid, and augmented binding of a growth factor. These observations suggest that the growth-promoting effect of vasopressin is not a simple function of its capacity to alter cell Na+ flux but could be mediated by other actions of the hormone, perhaps at the level of the plasma membrane.
Publisher
American Physiological Society
Cited by
40 articles.
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