Plasma Progesterone in Normal Subjects and Patients with Benign Essential Hypertension on Normal, Low, and High Sodium Intake1

Abstract

Plasma progesterone determined by a protein-binding method was significantly higher (p < 0.001) in 27 patients with stable BEH (79.0 ± 56.0 sd ng/100 ml) than in 21 healthy subjects (35.0 ± 14 sd ng/100 ml). Four out of 11 patients with labile hyperkinetic BEH had markedly increased plasma progesterone. However, the mean (59.0 ± 54.0 sd ng/100 ml) was statistically not different (p < 0.1) from control. Sodium restriction induced a marked increase in plasma progesterone in seven (out of eight) control subjects and in six out of 13 patients with BEH. The remaining one control and seven hypertensive patients showed a blunted response. Plasma progesterone in two of the control subjects returned to normal after sodium loading. Plasma cortisol determined by a protein-binding method remained the same after sodium depletion in eight normal and 15 patients with BEH. When patients with BEH were kept on normal diet, 13 of 15 determinations were below the mean value for control subjects. From comparison of these findings with published results on the relationship between aldosterone, angiotensin, progesterone and sodium excretion, it is concluded that the significant raise in plasma progesterone concentration associated with sodium restriction corresponds to the increase in renin-angiotensin in control subjects but not in all hypertensive patients. The cause for a raised basal progesterone level in many patients with BEH is not clear.