title: Responses of the renal prostanoids to a short-term depletion of sodium or potassium in healthy women.
abstract: The short-term effects of extracellular fluid volume depletion on the generation of some bioregulators of the renal function have been studied in healthy women. Eight subjects (SD group) were submitted to a low NaCl dietary intake and natriuretic treatment. At the end of the treatment (6 days) a cumulative sodium deficit of 381 +/- 55 mmol (mean +/- SEM) and a body weight variation of -2.1 +/- 0.28 kg were estimated. The renal function was explored by clearance method during hypotonic polyuria induced by oral water load and subsequent antidiuresis induced by low-dose infusion of lysine-8-vasopressin. The basal values of plasma renin activity were determined just before the water load as well as the urinary aldosterone excretion of the foregoing 24 hours was. During the renal functional exploration the urinary concentrations of PGE2, 6-keto-PGF1 alpha (6KPGF) and TxB2 were determined by RIA method. We report also, as comparison terms, the results obtained either in potassium depletion (KD group, n = 12) or in normal sodium and potassium balance (N group, n = 20). 1) In the SD vs N group-besides the increase in renin and aldosterone secretion-the behaviour of urinary prostanoids is consistent with a stimulation of the renal synthesis of PGI2 and TxA2 as well as of PGE2, at least as a trend. 2) In the KD vs N group an increase in renin secretion occurred while the urinary aldosterone was not significantly decreased. The urinary prostanoid data suggest an inhibition of the renal synthesis of PGE2 and PGI2. All three urinary prostanoids were significantly lower in the KD as compared to the SD group. Thus, in salt depletion the renal prostanoid synthesis was enhanced while it was depressed in potassium depletion, despite the increased renin secretion.
authors.affiliation: Cattedra di Medicina Interna II, Università di Bologna.
authors.forename: G C
authors.initials: GC
authors.lastname: Agnoli
authors.forename: R
authors.initials: R
authors.lastname: Borgatti
authors.forename: M
authors.initials: M
authors.lastname: Cacciari
authors.forename: C
authors.initials: C
authors.lastname: Garutti
authors.forename: E
authors.initials: E
authors.lastname: Ikonomu
authors.forename: P
authors.initials: P
authors.lastname: Lenzi
authors.forename: M
authors.initials: M
authors.lastname: Marinelli
authors.forename: L
authors.initials: L
authors.lastname: Stipo
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood; D000584:Amiloride / Q000494:pharmacology; D001835:Body Weight / Q000187:drug effects; D002752:Chlorthalidone / Q000494:pharmacology; D004039:Diet, Sodium-Restricted; D004232:Diuretics / Q000494:pharmacology; D005260:Female; D006706:Homeostasis; D006801:Humans; D006852:Hydrochlorothiazide / Q000494:pharmacology; D007008:Hypokalemia / Q000139:chemically induced / Q000378:metabolism*; D007010:Hyponatremia / Q000139:chemically induced / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D007677:Kidney Function Tests; D011141:Polyuria / Q000139:chemically induced / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D011453:Prostaglandins / Q000096:biosynthesis* / Q000652:urine; D012016:Reference Values; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D012964:Sodium / Q000378:metabolism*; D014867:Water
chemical_list: D004232:Diuretics; D011453:Prostaglandins; D014867:Water; D006852:Hydrochlorothiazide; D000450:Aldosterone; D000584:Amiloride; D012964:Sodium; D012083:Renin; D002752:Chlorthalidone; D011188:Potassium