Circadian rhythms of urinary sodium, potassium and some agents influencing their excretion in young borderline hypertensives.

The circadian rhythms of sodium (Na+), potassium (K+), aldosterone (ALDO), 11-deoxycorticosterone (DOC), 18-hydroxy-DOC (18-OH-DOC), cortisol (F), corticosterone (B), adrenaline (A), noradrenaline (NA), dopamine (DA), metanephrine (MN), normetanephrine (NMN), homovanillic acid (HVA), kallikrein (KE) and prostaglandins E (PGE) and F2 alpha (PGF2 alpha) excretion were studied in eight young borderline hypertensive men (BHT) and in six healthy age-matched normotensive subjects (NT) during hospitalization, after adaptation to the hospital regimen and a diet containing 135 mmol Na+ and 90 nmol K+. Urine samples were collected in 4 h periods for 24 h: 1. at normal daily activity, 2. during a 24 h bed rest. The results were evaluated by means of cosinor analysis. The circadian rhythms of ALDO, F, B, 18-OH-DOC and PGF2 alpha excretion were similar in both groups, with the exception of higher mesors of urinary ACTH-dependent corticosteroids in BHT at normal daily activity. Differences were observed in the rhythms of Na+, A, NA, DA, HVA and PGE excretion, this, however, above all during the normal daily regimen. The curve of urinary Na+ was flat in BHT due to a higher portion of Na+ excreted during the night. In the rhythms of A, NA and PGE excretion, the acrophases were shifted to the later hours in BHT, and the mesors of A and NA were also significantly higher. In contrast, DA and HVA excretion curves were flat with a lower mesor. These changes normalized, or at least mitigated, during a 24 h bed rest. The results of the study show that the circadian rhythm of Na+ excretion are disturbed already in the initial stage of hypertension. The likely cause is the exaggerated rise in adrenergic activity in the kidney during the day, induced by orthostasis and the concomitant physical (and mental?) activity, which is inadequately compensated for by the activation of natriuretic mechanisms.