Effects of experimental salt depletion on urinary prostanoid excretions in normal women.
The effects of moderate salt depletion on urinary excretions of prostanoids (PG)E2, 6-keto-PGF1alpha (6KPGF) and thromboxane (TX)B2 have been investigated in healthy women (SD group, n = 14). Salt depletion was obtained by combining a low sodium chloride dietary intake (< 60 mmol per day) with natriuretic and potassium sparing treatment. At the end of the treatment, the cumulative sodium deficit was 438 +/- 42 mmol (mean +/- SEM). Plasma renin activity (PRA) and urinary aldosterone excretion were determined in basal conditions. Renal functional exploration was performed during hypotonic polyuria (by oral water load) and subsequent moderate antidiuresis (by low dose infusion of an antidiuretic hormone analogue). In both phases, renal function was estimated by the clearance (cl.) method and the urinary concentrations of PGE2, 6KPGF and TXB2 by RIA method. The control group was composed of 20 healthy women in normal sodium and potassium balance (N group). Salt depletion was effective in increasing the basal values of plasma renin activity (PRA) and urinary aldosterone excretion. Moreover, it was effective in inducing the following during polyuria: (a) a depression of the diuretic response to water load in presence of a reduction in plasma osmolality; (b) a reduction in creatinine cl. in the absence of significant changes in mean arterial pressure; (c) an increase in the fractional reabsorption of sodium and chloride, in particular at the level of the diluting segments. Both in polyuria and in antidiuresis, the excretions of 6KPGF and TXB2 were higher in the SD vs. N group, while the excretion of PGE2 was not significantly different. In SD and N pooled groups, significant positive correlations were shown between basal PRA and urinary excretions during polyuria of 6KGPF and TXB2, (but not of PGE2) as well as between the excretions of the two metabolites. In conclusion, functionally effective salt depletion induces in healthy women a stimulation of renal synthesis of both prostacyclin and thromboxane. The excretory data do not give evidence of a similar effect on PGE2 synthesis.
Agnoli
G C
GC
Dipartimento di Medicina Interna, Cardioangiologia, Epatologia, Università di Bologna, Italy.
Borgatti
R
R
Cacciari
M
M
Lenzi
P
P
Marinelli
M
M
Stipo
L
L
D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000328:Adult; D000450:Aldosterone / Q000652:urine; D001790:Blood Physiological Phenomena; D002712:Chlorides / Q000378:metabolism; D004039:Diet, Sodium-Restricted; D015232:Dinoprostone / Q000652:urine; D005260:Female; D006801:Humans; D007668:Kidney / Q000502:physiology; D008875:Middle Aged; D009994:Osmolar Concentration; D011453:Prostaglandins / Q000652:urine*; D012083:Renin / Q000097:blood; D012964:Sodium / Q000097:blood / Q000172:deficiency*; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage; D013929:Thromboxane B2 / Q000652:urine; D014508:Urea / Q000378:metabolism; D014554:Urination
D002712:Chlorides; D011453:Prostaglandins; D017673:Sodium Chloride, Dietary; D000450:Aldosterone; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D014508:Urea; D012964:Sodium; D012083:Renin; D015232:Dinoprostone