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Interaction of aldosterone and oxytocin to influence renal sodium excretion in rats
Author(s) -
Musabayane CT,
Ndhlovu CE,
Forsling ML,
Balment RJ
Publication year - 1994
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1994.sp003806
Subject(s) - aldosterone , endocrinology , medicine , excretion , chemistry , oxytocin , adrenalectomy , mineralocorticoid , hormone , sodium , organic chemistry
The possibility of an interaction between oxytocin and aldosterone to influence renal Na+ excretion was investigated in Inactin‐anaesthetized male Sprague‐Dawley rats. Endogenous plasma concentrations of aldosterone were suppressed by either adrenalectomy or bicarbonate infusion. The effects of 2 h intravenous administration of oxytocin (0.04 pmol/min) and/or aldosterone (42 pmol/min) on renal Na+ handling were studied in 0.077 M NaCl‐infused adrenalectomized (Adx) rats and groups of intact animals that were infused with 0.077 M NaHCO3. Aldosterone alone significantly (P < 0.01) reduced Na+ excretion from pretreatment peak value of 5.0 +/− 1.0 to 1.5 +/− 0.4 mumol/min in Adx animals (n = 8) and 9.2 +/− 1.2 to 5.2 +/− 1.2 mumol/min in NaHCO3‐infused rats (n = 8) by 2 h after the start of administration. However, combined administration of aldosterone and oxytocin was associated with a significantly (P < 0.01) increased Na+ excretion rate from a peak pretreatment value of 6.8 +/− 0.7 mumol/min to a peak value of 11.5 +/− 1.1 mumol/min by 1 h 40 min after the start of treatment in Adx rats (n = 7). In bicarbonate‐infused rats (n = 8) Na+ excretion rose within 20 min of the start of treatment from a pretreatment peak of 9.0 +/− 0.8 mumol/min to a peak value of 13.5 +/− 0.8 mumol/min in response to combined hormone administration. In conclusion, we have shown that concomitant administration of aldosterone and oxytocin increased the rate of excretion of Na+ in two different preparations, which supports the idea of an interaction between the steroid and oxytocin to promote Na+ loss.