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.

[Differential aspects of the dynamics of the renin-angiotensin-aldosterone system in obesity with and without hypertension and in essential arterial hypertension]. / Aspetti differenziali della dinamica del sistema renina-angiotensina-aldosterone nell'obesità con e senza ipertensione e nella ipertensione arteriosa essenziale.

This report describes the impulsive function of the RAAS investigated in obese and non-obese hypertensives as compared to obese and non-obese normotensives. The aim of the investigation was to clarify whether or not the hypertensive vascular disease accompanying the ponderal excess can be regarded as a well-defined pathophysiologic entity. Data obtained showed that the behavior of the RAAS in hypertensive obese patients is quite different from that of non-obese hypertensives and obese normotensives. Such a difference implies that hypertension of obese people is a biochemically distinguishable entity. This observation corroborates the concept that the clinical association of obesity-hypertension might be regarded as a syndrome with a proper nosographic dignity.

Effect of ageing on circadian rhythms of plasma renin and aldosterone in mesor-hypertensive women.

This study investigated the changes in circadian rhythms of plasma renin activity (PRA) and plasma aldosterone (PA) which occur in essential mesor-hypertensive women, increasing in age. Systemic blood samples were taken throughout a 12 h period from both mesor-hypertensive women and clinically healthy women (control). The women in each group were either post-menopausal or had normal menstrual cycles. A cosinor method of temporal series was the analysis employed to compute the properties of PRA and PA circadian rhythms. The clearest effect of ageing, recorded in essential mesor-hypertensive women, is a decrease in circadian mesor of PRA cycle (P = 0.002). The age-related changes in clinically healthy women appear to be more extensive and involve a decrease for both mesor (P less than 0.001) and amplitude (P = 0.007) of PRA circadian rhythm. These disparities are convincing evidence for a non-physiological decline of the RAAS rhythmic function in the aged essential mesor-hypertensive women. The lack of an age-associated decrease in circadian PRA amplitude merits and pathophysiological and clinical investigation because it is a possible risk factor for post-menopausal, essential mesor-hypertensive women.

Inactive and active renins, aldosterone and cortisol in puerpera and newborn.

Eleven primiparae (aged from 20 to 31 years) have been sampled at the time of partum and throughout the puerperium for simultaneous determinations of plasma levels of inactive (prorenin) and active (PRA) renins, aldosterone (PA) and cortisol (PC). Biodata have been compared to time-qualified values obtained in non-pregnant adult women (aged from 17 to 37 years). Pregnant women show peripartum levels of prorenin, PRA, PA and PC significantly higher than the time-qualified reference intervals. Gestational increment is meanly of 3-4 times for prorenin, of 5-8 times for PRA, of 17-19 times for PA, of 4-5 times for PC. Puerperal levels of PRA, PA and PC show a progressive decline while those of prorenin suddenly fall and then remain quite stable. Neonatal levels of prorenin, PRA, PA and PC are higher than normal. Neonates show levels of prorenin, PRA, PA and PC, respectively equal, increased equal and decreased when compared to mothers. The different equipment of hormonal levels in mother and newborn leads to suggest a selective role of the placenta as a filter.

Ageing and circadian rhythm of plasma renin and aldosterone.

Five men and 8 women, 60-69 yr of age, and 4 men and 5 women, 17-37 yr of age, volunteered for this exploration of possible age-related changes in circadian-rhythm (CR) characteristics of radioimmunoassayable plasma renin (PRA) and aldosterone (PA). Blood was drawn at 06.00, 08.00, 12.00, 18.00, 20.00 and 24.00 from recumbent subjects on a habitual sodium intake of 120-140 mEq/24 h. Time-qualified data of PRA and PA, fitted by a 24-h cosine curve, were summarized by a population mean-cosinor method. Circadian characteristics were compared by a multivariate analysis using Hotelling's t2 test. Rhythmometry reveals in the elderly women a lower mesor (P less than 0.001) and amplitude (P = 0.036) of the CR in PRA and a higher mesor and amplitude (P = 0.021 and P = 0.020, respectively) of the PA-CR. The PRA acrophase is delayed (P less than 0.001) in the elderly women (04.40 vs. 08.04) while the timing of the PA acrophase is similar in the age groups of women compared (05.52 vs. 05.20). These differences found in women were not observed in the smaller groups of men. The seventh decade of life may be characterized by an internal circadian desynchronization between the major components of the renin-angiotensin-aldosterone system. A sex-dependent amplification of the extent of circadian variation in aldosterone may precede a decrease in the circadian amplitude occurring during the eighth decade of life, as a sign of the adrenopause in women.