Circadian Rhythm Of Aldosterone Research Articles

Inhaled corticosteroid therapy reduces the early morning peak in cortisol and aldosterone

1. As mineralocorticoid and adrenocorticoid activity are both under the diurnal control of adrenocorticotropic hormone secretion, we aimed to evaluate whether the normal circadian rhythm of cortisol and aldosterone secretion was suppressed by inhaled corticosteroid therapy.2.Ten normotensive patients with mild-moderate asthma, mean age 24.0 (S.D. 9.8) years and mean arterial pressure 90.7 (9.8) mmHg, were studied in a double-blind, randomized crossover design comparing placebo with fluticasone propionate, 1000 microgram administered twice daily at 08:00 h and 20:00 h. After 5 days of repeated dosing at steady state, measurements were made of plasma cortisol and aldosterone at midnight and 08:00 h.3. With placebo there was a significant (P<0.05) difference between cortisol values at 08:00 h (588.6+/-83.8 nmol/l) and midnight (109.6+/-35.0 nmol/l), whereas after treatment with fluticasone propionate there was no significant difference between levels at 08:00 h (143.3+/-57.4 nmol/l) and midnight (64.3+/-22.3 nmol/l). For cortisol at 08:00 h there was also a significant (P<0.05) difference between placebo and fluticasone propionate. The same pattern was observed for aldosterone. Plasma aldosterone levels at 08:00 h after treatment with placebo (129.6+/-30.9 nmol/l) were significantly different (P<0. 05) to those seen at midnight (40.4+/-6.2 nmol/l). After treatment with fluticasone propionate, there was no significant difference between levels at midnight (55.4+/-11.7 nmol/l) and 08:00 h (64. 8+/-12.7 nmol/l).4. These results show that inhaled corticosteroid therapy abolishes the circadian rhythm of aldosterone and cortisol secretion. This may have possible implications for patients taking inhaled corticosteroids in terms of the beneficial cardiac effects of suppressing early morning aldosterone.

Inhaled corticosteroid therapy reduces the early morning peak in cortisol and aldosterone

1.As mineralocorticoid and adrenocorticoid activity are both under the diurnal control of adrenocorticotropic hormone secretion, we aimed to evaluate whether the normal circadian rhythm of cortisol and aldosterone secretion was suppressed by inhaled corticosteroid therapy. 2.Ten normotensive patients with mild–moderate asthma, mean age 24.0 (S.D. 9.8) years and mean arterial pressure 90.7 (9.8) mmHg, were studied in a double-blind, randomized crossover design comparing placebo with fluticasone propionate, 1000 ;μg administered twice daily at 08:00 ;h and 20:00 ;h. After 5 days of repeated dosing at steady state, measurements were made of plasma cortisol and aldosterone at midnight and 08:00 ;h. 3.With placebo there was a significant (P&lt; 0.05) difference between cortisol values at 08:00 ;h (588.6±83.8 ;nmol/l) and midnight (109.6±35.0 ;nmol/l), whereas after treatment with fluticasone propionate there was no significant difference between levels at 08:00 ;h (143.3±57.4 ;nmol/l) and midnight (64.3±22.3 ;nmol/l). For cortisol at 08:00 ;h there was also a significant (P&lt; 0.05) difference between placebo and fluticasone propionate. The same pattern was observed for aldosterone. Plasma aldosterone levels at 08:00 ;h after treatment with placebo (129.6±30.9 ;nmol/l) were significantly different (P&lt; 0.05) to those seen at midnight (40.4±6.2 ;nmol/l). After treatment with fluticasone propionate, there was no significant difference between levels at midnight (55.4±11.7 ;nmol/l) and 08:00 ;h (64.8±12.7 ;nmol/l). 4.These results show that inhaled corticosteroid therapy abolishes the circadian rhythm of aldosterone and cortisol secretion. This may have possible implications for patients taking inhaled corticosteroids in terms of the beneficial cardiac effects of suppressing early morning aldosterone.

Circadian rhythms of hypothalamic norepinephrine and of some circulating substances in individually housed adult rats

The circadian rhythms of hypothalamic norepinephrine (NE) and of circulating norepinephrine, epinephrine (E), corticosterone, aldosterone, and serotonin (5HT) were determined in group-housed and in individually housed male adult rats, adapted to a 12/12 light/dark cycle. After 5 weeks of individual housing, compared to group-housed animals, hypothalamic NE mesor decreased, while circulating NE, E, and corticosterone mesor increased. The circadian rhythms of aldosterone and 5HT were unaffected by individual housing.

Chronobiological Evidence for an Uncoupling of the Na,K-ATPase to Aldosterone in Normal Renin Hypertension

The Na,K-ATPase activity of erythrocyte membranes is markedly increased in normal-renin essential hypertensives. A temporal shift of the chronobiology of the erythrocyte-membrane-bound Na,K-ATPase in these patients is described. The disorder causes a loss of synchronism between the circadian rhythms of aldosterone and Na,K-ATPase. Such uncoupling phenomenon may explain the inversion of the day/night sodium excretion ratio and other disturbances of sodium metabolism found in essential hypertensives.

Effects of a mild and prolonged restriction in sodium or food intake on the circadian rhythm of aldosterone and related variables.

The effect of a mild reduction in dietary sodium intake (-30 mEq/24 hr) and body weight (-2 kg/2 months) on circadian rhythms of urinary aldosterone (UA), sodium (UNa), potassium (UK), creatinine (UC) and volume (UV) have been investigated in nine clinically healthy subjects. The mild reduction in dietary sodium is associated with: (1) a decrease in the 24-hr excretion rate of UNa, UK and UV, and an increased mesor of UA and UC; (2) a lowered extent of the circadian variation for UNa, UK, UV and a greater amplitude for UA and UC (3) a later crest in the temporal phase for UK, UA, UC, an earlier phasic wave for UNa. The mild reduction in calorie intake resulting in a body weight loss is associated with a more pronounced decrease in the 24-hr excretion rate of UNa and UK, and in the extent of circadian fluctuation for UNa. Peculiar events are: (1) the decreased 24-hr excretion rate for UA, and the increased mesor for UV; (2) the extent variability increased for UV, decreased for UC. Such effect may have a practical resonance for heuristic physiology since the role of dietary sodium and food intake has been better clarified. Dietary sodium and food can be regarded as 'chronomodulatory agents' for the adrenal cortex since their adrenotropic influence is extended to the tonic as well as phasic secretion of aldosterone.

Plasma cortisol and aldosterone after ACTH 1-17: effect of different doses.

In order to evaluate the effects in adults of different doses of ACTH 1-17 on the cortisol and aldosterone secretion, 200 micrograms of ACTH 1-17 were injected i.m. at 07(00) in two groups of 6 patients each of both sexes. Sampling was done before and after ACTH 1-17 administration at 4-h intervals from 08(00) to 04(00) in order to define the circadian profiles of both cortisol and aldosterone. At the time of study all subjects were kept under the same routine conditions. The i.m. injection of 100 micrograms of ACTH 1-17 was followed by a maximum response of cortisol which coincided with the physiological circadian peak of the hormone (511.7 +/- 122.7 vs 195.5 +/- 92.9 ng/ml; mean +/- 1 SD; p less than 0.001). With this treatment no variations in the normal circadian rhythm were observed. After the injection of 200 micrograms ACTH 1-17, a marked variation in the circadian rhythm of cortisol (peak at 16(00): 390.0 +/- 49.8 ng/ml; mean +/- 1 SD) was observed. Significant variations in the circadian rhythm of aldosterone with respect to the normal profile were observed only after the injection of 200 micrograms ACTH 1-17 (peak at 16(00): 137.5 +/- 50.5 vs 50.8 +/- 36.1 ng/ml; mean +/- 1 SD; p less than 0.01). The hormone increase observed after the injection of 100 micrograms (peak at 08(00): 111.7 +/- 87.5 vs 61.3 +/- 16.5 ng/ml; mean +/- 1 SD) was not statistically significant. Our results indicate that the clinical use of ACTH 1-17 i.m. is not recommended at doses greater than 100 micrograms.(ABSTRACT TRUNCATED AT 250 WORDS)

Rhythm characteristics of plasma renin, aldosterone and cortisol in five subtypes of mesor-hypertension.

The possible role of the renin-angiotensin system and ACTH in controlling the temporal organization of circadian rhythm of aldosterone was studied in patients with mesor-hypertension (MH) by simultaneous radioimmunological determinations of within-day changes in plasma renin, aldosterone and cortisol. Thirty-nine uncomplicated, untreated mesor-hypertensive patients, divided in subtypes, were examined. The interrelationship between the rhythm components revealed that the circadian cyclicity of aldosterone in both mesor-normotensive and mesor-hypertensive subjects, with either normal or high renin patterns, has a similar timing in acrophase with renin periodicity, which leads the circadian cortisol rhythm. In low-renin mesorhypertensive subjects a circadian rhythm of aldosterone and cortisol, but not of renin, remains demonstrable. The confidence limits of the estimated acrophase for circadian cortisol rhythm do not, however, overlap the confidence arcs of the aldosterone phase. These findings suggest that in normal or high renin MH subjects the aldosterone rhythmicity is mainly controlled by the renin-angiotensin system. Conversely in low-renin MH subjects the temporal organization of the aldosterone circadian sequences seems to be completely independent of renin-angiotensin control.