Fibroblast Na+-Li+ countertransport rate is elevated in essential hypertension

Citation
G. Zerbini et al., Fibroblast Na+-Li+ countertransport rate is elevated in essential hypertension, J HYPERTENS, 19(7), 2001, pp. 1263-1269
Citations number
48
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF HYPERTENSION
ISSN journal
02636352 → ACNP
Volume
19
Issue
7
Year of publication
2001
Pages
1263 - 1269
Database
ISI
SICI code
0263-6352(200107)19:7<1263:FNCRIE>2.0.ZU;2-L
Abstract
Objectives Elevated erythrocyte Na+-Li+ countertransport (SLC) rates are co mmonly found in essential hypertension. We have recently shown that human s kin fibroblasts functionally express a phloretin-sensitive Na+-H+ exchange (NHE) which may also be similar to erythrocyte SLC because of amiloride-ins ensitivity. Design and methods We investigated whether elevations in fibroblast SLC par allel the known elevations in erythrocyte SLC and in cell NHE that characte rize essential hypertension, Results Higher fibroblast SLC rates were found among hypertensive patients (n = 23, median 48.8 nmol Li+/mg(protein) per min) than in 19 normotensive individuals of similar age and sex (median 14.8 nmol Li+/mg(protein) per mi n, P = 0.0002). As expected, erythrocyte SLC was elevated in patients with hypertension (median 411 versus 329 mu mol/l(cell) per h, P = 0.0273), but was not quantitatively related to fibroblast SLC, Finally, fibroblast NHE e xchange activity was higher in essential hypertension (median V-max 14.2 ve rsus 7.6 mmol H+/I-cell per min, P = 0.002), but was unrelated to fibroblas t SLC. Conclusions These findings extend to human skin fibroblasts the notion of a bnormal Li+ transport in essential hypertension, and appear to be in accord ance with the hypothesis that fibroblast SLC may be independent of NHE, How ever, molecular studies will be required to understand whether distinct exc hangers and/or regulation mechanisms underlie these dysregulations. (C) 200 1 Lippincott Williams & Wilkins.