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Query: UMLS:C0085580 (
essential hypertension
)
14,686
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Primary aldosteronism (PA) is the most common cause of endocrine hypertension with a high frequency of cardiovascular complications. The unfavorable cardiometabolic profile may be due to aldosterone-mediated activation of inflammatory cells, circulatory cytokines and activation of collagen synthesis in the vessel wall. Aim of our study was to evaluate differences in the levels of hsCRP, IL-6, TNF-alpha and N-terminal propeptide of collagen I (PINP) in patients with PA and
essential hypertension
(EH) as a control group, and between the subtypes of PA (aldosterone producing adenoma -
APA
, idiopathic hyperaldosteronism - IHA). We studied 28 patients with PA (IHA - 10 patients,
APA
- 12 patients, 6 unclassified) and 28 matched patients with EH. There were no differences in the levels of inflammatory markers between the followed groups [EH vs. PA: TNF-alpha (5.09 [3.68-6.32] vs. 4.84 [3.62-6.50] pg/ml), IL-6 (0.94 [0.70-1.13] vs. 0.97 [0.71-1.28] pg/ml), hsCRP (0.53 [0.25-1.54] vs. 0.37 [0.31-0.61] mg/l), leukocytes (6.35+/-1.42 vs. 5.97+/-1.29 10(9) l);
APA
vs. IHA: TNF-alpha (4.54 [3.62-7.03] vs. 5.19 [4.23-5.27] pg/ml), IL-6 (0.96 [0.63-1.21] vs. 0.90 [0.65-1.06] pg/ml), hsCRP (0.34 [0.29-0.47] vs. 0.75 [0.36-1.11] mg/l), leukocytes (6.37+/-1.41 vs. 5.71+/-1.21 10(9) l)]. Significant differences in the levels of PINP between PA and EH group were observed (35.18 [28.46-41.16] vs. 45.21 [36.95-62.81] microg/l, p</=0.003). No differences in inflammatory markers were observed between the followed groups, we confirmed higher levels of PINP in patients with PA.
...
PMID:Inflammatory markers in primary aldosteronism. 2644 10
Obesity is assumed to be a major cause of human
essential hypertension
; however, the mechanisms responsible for weight-related increase in blood pressure (BP) are not fully understood. The prevalence of hypertension induced by obesity has grown over the years, and the role of the renin-angiotensin-aldosterone system (RAAS) in this process continues to be elucidated. In this scenario, the
ob/ob
mice are a genetic obesity model generally used for metabolic disorder studies. These mice are normotensive even though they present several metabolic conditions that predispose them to hypertension. Although the normotensive trait in these mice is associated with the poor activation of sympathetic nervous system by the lack of leptin, we demonstrated that
ob/ob
mice present massively increased
aminopeptidase A
(
APA
) activity in the circulation.
APA
enzyme metabolizes angiotensin (ANG) II into ANG III, a peptide associated with intrarenal angiotensin type 2 (AT
2
) receptor activation and induction of natriuresis. In these mice, we found increased ANG-III levels in the circulation, high AT
2
receptor expression in the kidney, and enhanced natriuresis. AT
2
receptor blocking and
APA
inhibition increased BP, suggesting the ANG III-AT
2
receptor axis as a complementary BP control mechanism. Circulating
APA
activity was significantly reduced by weight loss independently of leptin, indicating the role of fat tissue in
APA
production. Therefore, in this study we provide new data supporting the role of
APA
in BP control in
ob/ob
mouse strain. These findings improve our comprehension about obesity-related hypertension and suggest new tools for its treatment.
NEW & NOTEWORTHY
In this study, we reported an increased angiotensin III generation in the circulation of
ob/ob
mice caused by a high
aminopeptidase A
activity. These findings are associated with an increased natriuresis found in these mice and support the role of renin-angiotensin-aldosterone system as additional mechanism regulating blood pressure in this genetic obese strain.
...
PMID:High aminopeptidase A activity contributes to blood pressure control in
ob/ob
mice by AT
2
receptor-dependent mechanism. 2794 Sep 65
Primary aldosteronism is the most common type of secondary hypertension affecting 6-10% of patients with
primary hypertension
. PA is mainly caused by unilateral hyperaldosteronism due to an aldosterone-producing adenoma, unilateral hyperplasia with or without micronodules or bilateral zona glomerulosa hyperplasias with or without macro or micronodules. The development of antibodies against the terminal enzyme of aldosterone biosynthesis (CYP11B2) has permitted the further characterization of normal adrenals and resected adrenals from patients with primary aldosteronism. Normal adrenals exhibit two different patterns of cellular expression of CYP11B2: young individuals display a relatively uniform expression of the enzyme throughout the zona glomerulosa while the adrenals of older individuals have dispersed CYP11B2-expressing cells but have more groups of cells called aldosterone-producing cell clusters (APCC). APAs exhibit different patterns of CYP11B2 staining that vary from uniform to homogeneous. There are also a proportion of cells within the
APA
that co-express different enzymes that are not normally co-expressed in normal individuals. Approximately 30% of patients with unilateral hyperaldosteronism do not have an
APA
, but either have an increased number of CYP11B2 expressing micronodules or hyperplasia of the zona glomerulosa. In summary, the studies reported in this review are shedding new light on the pathophysiology of primary aldosteronism. The wide variation in histopathological features of the adenomas and concurrent presence of APCCs raises the possibility that most cases of unilateral production of aldosterone actually might represent bilateral asymmetric hyperplasia with nodules frequently due to the development of somatic aldosterone-driving mutations.
...
PMID:Disordered CYP11B2 Expression in Primary Aldosteronism. 2920 95
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