| pubmed-article:7755470 | pubmed:abstractText | We have recently described that urines from salt-loaded rats contain a potent natriuretic factor acting at the Na-K-Cl cotransport system (CIF: "Cotransport Inhibitory Factor"). Here we investigated the kinetics of the urinary CIF excretion which follows an oral salt-load: (i) in normal rats, relative to that of the atrial natriuretic peptide (ANP) and (ii) in an experimental model of salt-dependent genetic hypertension (Dahl's rats). Thus, Wistar rats were orally loaded with 2% NaCl for 8 days. Urinary CIF excretion was measured by testing the inhibitory potency of urines on bumetanide-sensitive lithium efflux in lithium-loaded human erythrocytes. Plasmatic levels of ANP were measured by radioimmunoassay. Plasma ANP rapidly and transiently increased during the first 24 hs of salt-load, decreasing thereafter down to normal levels in 6-8 days. Conversely, CIF slowly increased after 24 hs up to maximal constant levels after 5 days of salt-loading. Dahl salt-sensitive rats exhibited highly significant increases in urinary CIF excretion with respect to salt-resistant rats. In the basal state (before salt-loading) urinary CIF excretion was 101 +/- 13 vs 17.6 +/- 4.5 units/day in salt-sensitive vs. salt-resistant rats (n = 7 for each group, p < 0.001). This difference was maintained after salt loading (3 380 +/- 990 vs. 456 +/- 159 units/day, p < 0.05 at day 5).(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
