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STEVEN L. RABINOWE, TERRY TAYLOR, MIGUEL RUIZ, ROBERT G. DLUHY, GORDON H. WILLIAMS, β-Endorphin Stimulates Plasma Renin and Aldosterone Release in Normal Human Subjects, The Journal of Clinical Endocrinology & Metabolism, Volume 60, Issue 3, 1 March 1985, Pages 485–489, https://doi.org/10.1210/jcem-60-3-485
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Abstract
To determine the effect of β-endorphin on the renin-angiotensin-aldosterone system, human synthetic β3-endorphin (0.3, 1.0, and 3.0 µg⁄kg-min) was infused iv in normal subjects. Each dose was administered for 30 min, and a control infusion of 5‰ dextrose and water was given on another day.
Ten subjects were studied recumbent and in balance while ingesting a 10-meq Na+ diet. Plasma renin activity (PRA), plasma aldosterone (PA), and plasma cortisol (F) were measured basally and every 30 min for 210 min. The increments in PRA and PA above basal significantly (P < 0.05) increased (3.1 ± 1.2 ng⁄ml-h and 12.2 ± 5.3 ng⁄dl, respectively; P < 0.05) at the end of the β-endorphin infusion. β-Endorphin also significantly (P < 0.01) suppressed F levels.
Since in the low salt study, β-endorphin suppressed F release while stimulating renin secretion, an additional five subjects were pretreated with dexamethasone (0.5 mg every 6 h) and were studied in balance while ingesting a 200-meq Na+ diet to suppress the renin-angiotensin system. Significant (P < 0.025) increments in PRA (2.1 ± 0.7 ng⁄ml-h) and PA (4.1 ± 1.7 ng⁄dl) levels above basal were again found during the sequential dose infusion of β-endorphin (0.3,1.0, and 3.0 µg⁄kg-min). However, PA elevations were sustained for at least 120 min after the 0- endorphin infusion was stopped despite a drop in PRA 90 min earlier. In additional studies, an attempt was made to define the minimal effective dose of/3-endorphin by 60-min infusions (0.03, 0.1, and 0.3 µg⁄kg-min) in subjects on a 200-meq Na+ diet who were dexamethasone pretreated. The PRA and PA levels rose significantly (P < 0.05) above basal at the 0.3 µg⁄kgmin dose, but not at the 0.03 or 0.1 µg⁄kg-min dosage levels. There were no changes in blood pressure or potassium during either the 10 or 200-meq Na+ studies. Thus, β-endorphin stimulates aldosterone release in vivo. However, the underlying mechanisms are complex, since renin levels also increased. The data suggest that the early aldosterone rise may be secondary to an increase in renin release, but renin cannot account for the sustained postinfusion elevations of aldosterone.
