Sodium restriction amplifies and propranolol loading inhibits circadian rhythm of plasma renin-angiotensin and aldosterone.
Five male and 5 female clinically healthy volunteers, 17-37 years of age, gave systemic venous blood at 0600, 0800, 1200, 1800, 2000 and 0000 for RIA of (supine values) plasma renin-angiotensin (PRA) and aldosterone (PA) under 4 conditions: a. unrestricted sodium intake, no treatment; b. unrestricted sodium intake and 40 mg propranolol per os every 6 h; c. sodium restriction, no treatment; d. propranolol loading on sodium deprivation. Cosinor methods were used for data analysis. Sodium restriction amplifies the circadian rhythms of PRA and PA, whereas propranolol loading inhibits these same rhythms on a unrestricted sodium intake, but much less so under conditions of sodium deprivation. The propranolol-induced inhibition of the circadian rhythms investigated on a unrestricted sodium intake suggests that the beta-adrenergic system is an effective mechanism coordinating the circadian rhythmic functions investigated. The persistence of the rhythms in sodium-depleted subjects under pharmacological blockade of beta-adrenoreceptors is in keeping with the concept that a second mechanism of the circadian rhythms examined is located in the sodium-sensitive macula densa cells of the renal distal tubule.
Cugini
P
P
Halberg
F
F
Sothern
R B
RB
Centanni
M
M
Salandi
E
E
Scavo
D
D
D000293:Adolescent; D000328:Adult; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000097:blood*; D002940:Circadian Rhythm / Q000187:drug effects*; D004039:Diet, Sodium-Restricted; D005260:Female; D006801:Humans; D007606:Juxtaglomerular Apparatus / Q000187:drug effects; D008297:Male; D011433:Propranolol / Q000494:pharmacology*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects; D012083:Renin / Q000097:blood*
D011943:Receptors, Adrenergic, beta; D000804:Angiotensin II; D000450:Aldosterone; D011433:Propranolol; D012083:Renin