title: Renal, intestinal, and adrenal responses to sodium loading in Dahl-Iwai salt-sensitive and salt-resistant rats.
abstract: This study compared renal and intestinal handling of sodium in Dahl-Iwai salt-sensitive (S) and salt-resistant (R) rats given a normal-salt diet (0.3% NaCl) and a high-salt diet (4.0% NaCl). Six-week-old female S and R rats (n = 7 each) were given a normal-salt diet for 14 days followed by a high-salt diet for 3 weeks. Systolic blood pressure was significantly higher in the S rats than in the R rats only at the end of the high-salt diet period (170 +/- 5, mean +/- SEM, vs 152 +/- 1 mmHg, p < 0.01). Daily sodium intake, water intake, urine volume, and urinary and fecal excretions did not significantly differ between the R and the S rats during the normal- and high-salt diets, except for a slight, although significant, decrease in fecal sodium excretion in the S rats as compared with the R rats in the 2nd week of the high-salt diet period. After switching from the normal-salt diet to the high-salt diet, urinary sodium excretion increased by 17- to 18-fold and fecal sodium excretion increased by about 5-fold in the 1st week of salt loading. The changes in urinary and fecal sodium excretions did not differ significantly between the groups. Cumulative sodium retention was similar in the two groups. The aldosterone/creatinine ratio in 24-hr urine, which was significantly lower in the S than in the R rats during the normal-salt diet, decreased to similar levels in both groups after salt loading, indicating a blunted response of aldosterone in the S rats. Thus, there were no discernible differences in renal and intestinal handling of sodium between the S and the R rats, except for a slight, but significant, difference in fecal sodium excretion in the 2nd week of the high-salt period. The results indicate that inappropriate suppression of aldosterone or some other mechanism induced by salt loading may be involved in blood pressure elevation in Dahl-Iwai S rats.
authors.affiliation: Second Department of Internal Medicine, Yokohama City University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Katoh
authors.forename: S
authors.initials: S
authors.lastname: Umemura
authors.forename: K
authors.initials: K
authors.lastname: Sugimoto
authors.forename: M
authors.initials: M
authors.lastname: Tomiyama
authors.forename: Y
authors.initials: Y
authors.lastname: Abe
authors.forename: N
authors.initials: N
authors.lastname: Hirawa
authors.forename: M
authors.initials: M
authors.lastname: Ishii
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects* / Q000502:physiology; D000450:Aldosterone / Q000502:physiology / Q000652:urine; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D003404:Creatinine / Q000652:urine; D004326:Drinking; D004351:Drug Resistance; D005260:Female; D007422:Intestines / Q000187:drug effects* / Q000502:physiology; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D009318:Natriuresis; D051381:Rats; D011919:Rats, Inbred Strains; D012982:Sodium, Dietary / Q000008:administration & dosage* / Q000494:pharmacology / Q000652:urine
chemical_list: D012982:Sodium, Dietary; D000450:Aldosterone; D003404:Creatinine