SeminarMineralocorticoid hypertension
Section snippets
Mineralocorticoid secretion and hormone action
Adrenal corticosteroids are classified as mineralocorticoid or glucocorticoid. Both types of hormone are secreted from the adrenal cortex-glucocorticoids in large amounts (cortisol 10–20 mg daily) from the zona fasciculata, mineralocorticoids in small amounts (aldosterone 100–150 μg daily) from the zona glomerulosa. In normal physiology, aldosterone secretion is principally controlled by the renin-angiotensin system and stimulates sodium transport across epithelial cells in the distal nephron,
Primary aldosteronism
First described by Conn,11 primary aldosteronism is likely to be the most common cause of mineralocorticoid hypertension. Prevalence rates of 0·5-2·0% have been reported in unselected patients with essential hypertension,12 but many of these studies relied on detection of hypokalaemia and underestimated true prevalence rates. By contrast, studies in specialist centres showed high prevalence rates of 5–12% in hypertensive populations,13 but these studies were subject to selection bias.
Symptoms
Monogenic hypertension
Hypertension is a phenotype of some well-documented gene mutations. 17α-hydroxylase deficiency and 11β-hydroxylase deficiency are forms of congenital adrenal hyperplasia in which mineralocorticoid excess occurs because of corticotropin-driven deoxycorticosterone excess. A similar process is thought to explain hypertension in patients with glucocorticoid resistance due to mutations in the glucocorticoid-receptor gene (panel). More recently, a significant advance in understanding of the molecular
Diagnosis of mineralocorticoid-based hypertension
Wherever possible, an explanation of the underlying basis of a patient's hypertension should be sought, so that appropriate therapy can be given. At present, the incidence of primary aldosteronism, glucocorticoid-suppressible hyperaldosteronism, Liddle's syndrome, and apparent mineralocorticoid excess in unselected community-based rather than hospital-based populations of patients with essential hypertension is unknown. Until this incidence is known, the decision on who should and should not be
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The adrenal gland in stress – Adaptation on a cellular level
2019, Journal of Steroid Biochemistry and Molecular BiologyCitation Excerpt :Furthermore, they express the aldosterone synthetase CYP11B2, which converts corticosterone to aldosterone [24,25]. Aldosterone, which is synthesized under the control of the renin angiotensin-aldosterone system (RAAS), is the most potent mineralocorticoid involved in maintenance of water and sodium homeostasis and subsequently blood pressure adjustments [26]. The zF is comparatively bigger than the zG, and the zF cells are larger and less densely packed than the zG cells with a highly abundant smooth ER.
Glucocorticoid metabolism and activation
2018, Encyclopedia of Endocrine DiseasesPhosphodiesterase-4 inhibitors ameliorates cognitive deficits in deoxycorticosterone acetate induced hypertensive rats via cAMP/CREB signaling system
2015, Brain ResearchCitation Excerpt :One-way ANOVA revealed no significant changes in BDNF levels in the hippocampus of the clonidine treated rats. In the present study, the authors used the DOCA salt-induced hypertension model, a mineralocorticoid-based model of hypertension in rats which mimics "essential" hypertension in the clinical setting (Stewart, 1999; Hacioglu et al., 2003). The SBP, right kidney weight, heart weight and the heart index in DOCA salt-induced hypertensive rats were found to be significantly increased when compared to the sham operated group.
Primary Mineralocorticoid Excess Disorders and Hypertension
2015, Endocrinology: Adult and Pediatric