Aldosterone and stress-dependent arterial hypertension

Secretory activity of the adrenal cortex and hormonal reaction to emotional stress were examined in normotensive WAG and hypertensive ISIAH rats. Under nembutal narcosis (surgical stage), secretion of corticosteroid hormones and hormonal reaction to acute stress in hypertensive rats were enhanced. In these rats, the stress-induced elevation of aldosterone secretion was most pronounced, which indicates an important contribution of this hormone to the pathogenesis of stress-dependent arterial hypertension.     

Obstructive Sleep Apnea and Aldosterone

Background:

Obstructive sleep apnea (OSA) is a major risk factor for hypertension and has been associated with increased risk for cardiovascular morbidity. A dysregulated renin-angiotensin-aldosterone system may contribute to excess sodium retention and hypertension and may be activated in OSA. We tested the hypothesis that serum levels of aldosterone and plasma renin activity (PRA) are increased by apneic sleep in subjects without cardiovascular disease, compared to healthy control subjects.

Methods and Results:

Plasma aldosterone level was measured in 21 subjects with moderate to severe OSA and was compared to 19 closely matched healthy subjects. Plasma renin activity (PRA) was measured in 19 OSA patients and in 20 healthy controls. Aldosterone and PRA were measured before sleep (9pm), after 5 hrs of untreated OSA (2am) and in the morning after awakening (6am). There were no baseline (9pm) differences in serum aldosterone levels and PRA between the healthy controls and OSA patients (aldosterone: 55.2 ± 9 vs 56.0 ± 9 pg/mL; PRA: 0.99 ± 0.15 vs 1.15 ± 0.15 ng/mL/hr). Neither several hours of untreated severe OSA nor CPAP treatment affected aldosterone levels and PRA in OSA patients. Diurnal variation of both aldosterone and PRA was observed in both groups, in that morning renin and aldosterone levels were higher than those measured at night before sleep.

Conclusions:

Our study shows that patients with moderate to severe OSA without co-existing cardiovascular disease have plasma aldosterone and renin levels similar to healthy subjects. Neither untreated OSA nor CPAP treatment acutely affect plasma aldosterone or renin levels.

Citation:

Svatikova A; Olson LJ; Wolk R; Phillips BG; Adachi T; Schwartz GL; Somers VK. Obstructive sleep apnea and aldosterone. SLEEP 2009;32(12):1589-1592.     

Aldosterone in salt-sensitive hypertension and metabolic syndrome

Metabolic syndrome, which is caused by obesity, is now a global pandemic. Metabolic syndrome is an aggregation of hypertension, diabetes and dyslipidaemia. Insulin resistance is a key factor in the development of these components of metabolic syndrome. Concerning the mechanism for the development of hypertension in metabolic syndrome, the lack of insulin resistance in the kidney increases sodium reabsorption by hyperinsulinaemia, leading to sodium retention in the body, and resultant salt-sensitive hypertension. Moreover, hyperaldosteronism, which is caused by adipocyte-derived aldosterone-releasing factors, induces not only salt-sensitive hypertension, but also proteinuria in obese hypertensive rats. Salt loading markedly aggravates proteinuria and induces cardiac diastolic dysfunction in obese hypertensive rats, suggesting that salt and aldosterone exert unfavourable synergistic actions on the cardiovascular system, possibly through the overproduction of oxidative stress. In turn, reactive oxygen species (ROS), which are induced by adipokines such as tumour necrosis factor-α, non-esterified fatty acids, angiotensinogen etc., can activate the mineralocorticoid (MR) receptor, in an aldosterone-independent fashion. Therefore, aldosterone/MR activation plays a key role not only in the development of salt-sensitive hypertension, but also in cardiovascular injury in metabolic syndrome, possibly through its function as a feed-forward system.     

Aldosterone reverses potassium-induced food aversions in adrenalectomized rats

Young adult male rats were individually housed and given a standard ration (66 ml) of a liquid diet (Nutrament) each day. The animals were divided into 7 groups: five groups were bilaterally adrenalectomized (ADX) and given one of 5 doses of aldosterone and/or dexamethasone by continuous, osmotic minipump infusions. The remaining two groups served as intact and sham operated controls. Each of the seven groups were subdivided into 3 dietary groups: a basal potassium dietary group, a moderately potassium-supplemented dietary group, and a highly potassium-supplemented dietary group. All rats with intact adrenals as well as those ADX rats given basal or 10 X basal aldosterone treatment consumed all of their allotted 66 ml of diet each day, independent of the level of potassium supplementation. ADX rats given little or no aldosterone treatment that were given access to the moderately or highly supplemented diets became anorexic, eating little or none of the diet. These data are discussed with reference to the factors controlling the intake of ADX rats.