Page 85 - GPD-1-2

Gene & Protein in Disease Diagnosis and treatment of aldosterone-related diseases

control group, and the fasting blood glucose and glucose 2.5. Relationship between aldosterone and obesity
tolerance of the mice in the HC group were significantly It is still unclear whether elevated aldosterone levels in the
reduced. Furthermore, the insulin levels of the mice in both body lead to obesity or whether obesity leads to elevated
the HC and SO groups were significantly higher than those aldosterone levels. Studies have yet to determine which
in the control group. Significant reductions in aldosterone factor is the cause and which is the effect. In a study, obese
were also found in both the HC group and the SO group patients who had excess aldosterone before losing weight
compared to the control group. The increase in aldosterone continued to have lower plasma aldosterone levels after
may lead to impaired glucose tolerance, decreased islet losing weight . There are also studies that have investigated
[18]
ß-cell function, decreased insulin sensitivity to tissues, and the correlation between fat tissue and aldosterone in obese
thus increase the risk of diabetes. The study also confirmed men and women with normal blood pressure. The findings
that aldosterone levels are closely related to the action of revealed that only the aldosterone levels in women were
insulin and RAAS plays a key role in diabetes . significantly positively correlated with adipose tissue and
[15]
2.3. Relationship between aldosterone and body mass index (BMI) independently of renin. The study
atherosclerosis raised a possibility for investigating the sex-specific effect
of adipose tissue on aldosterone .
[19]
PA increases the risk of cardiovascular disease (CVD)
and independent of blood pressure. Animal models have In obese patients, the level of leptin is significantly
suggested that aldosterone accelerates atherosclerosis increased. Leptin can increase the aldosterone level
[20]
through pro-inflammatory changes in innate immune through RAAS and adrenal spherical cells . Studies
cells [16] . According to the study, patients with PA are have shown that leptin stimulates sympathetic activity by
more likely to develop atherosclerotic cardiovascular releasing renin through β-adrenaline receptors and the
events compared to essential hypertension. This sympathetic nervous system activates RAAS by elevating
[21]
suggests that chronic exposure to high aldosterone angiotensinogen in nerve tissue . Renin can also act with
levels, which is increasingly prevalent, has adverse adrenal globular band cells to enhance the expression
effects on the cardiovascular system. A growing number of CYP11B2 (cytochrome P450, subfamily XIB, and
of clinical studies have also emphasized that excessive polypeptide 2 gene) by relying on the signaling pathway
activation of RAAS not only leads to hypertension, of calcineurin, thereby promoting elevated aldosterone
[22]
but also causes atherosclerosis, congestive heart levels . In addition, since aldosterone impairs the insulin
failure, and other diseases [17] . The activation of MR in signaling pathway only at concentrations that may activate
endothelial cells promotes infiltration of inflammatory glucocorticoid receptors, elevated aldosterone levels
cells, followed by inflammation and fibrosis. The may also reduce insulin sensitivity in fat cells. However,
infiltrating macrophages engulf oxidized low-density the direct relationship between the two is still being
lipoprotein and become foam cells, thereby promoting studied [23,24] .
atherosclerosis .
[9]
3. Diagnostic methods for aldosterone-
2.4. Relationship between aldosterone and chronic related diseases
kidney disease
Aldosterone is a steroid hormone. Since the levels of steroid
Chronic kidney disease (CKD) is also a significant public hormones in the body are extremely low, the general
health concern. Based on evidence, the excessive activation detection level is in nmol/L or pmol/L, which increases
of RAAS is one of the key pathogeneses in its complex the difficulty of clinical diagnostic testing. At present, PA is
pathophysiology. RAAS is distributed throughout the blood considered one of the most common causes of hypertension.
vessel walls, heart, kidneys, and other organs of the body, Hiramatsu et al. first introduced the aldosterone-renin
but the kidneys, which secrete renin, are the initial organs ratio (ARR) as an indicator of PA screening . Although
[25]
[9]
of the RAAS . Therefore, when RAAS is overactivated, ARR is now an important screening method for the
renin secretion increases, which, in turn, stimulates diagnosis of PA, the high false-positive rates exhibited by
angiotensin I receptors, leading to vascular endothelial ARR methods are a concern. Therefore, each measurement
cell growth, oxidative stress, and vascular inflammation. of aldosterone and renin as well as the calculated ARR
This exacerbates arterial stiffness and accelerates vascular value is all extremely important . According to another
[26]
aging. The increased angiotensin II and aldosterone levels piece of evidence, low renin activity or concentrations are
may promote cardiomyocyte inflammation, fibrosis, and seen in the majority of hypertensive individuals, especially
hypertrophy, leading to cardiovascular remodeling and when renin levels are undetectably low, and aldosterone
dysfunction . concentrations are also significantly lower than normal .
[17]
[27]
Volume 1 Issue 2 (2022) 3 https://doi.org/10.36922/gpd.v1i2.136