Disease relevance of Hyperaldosteronism

• To test the hypothesis that idiopathic hyperaldosteronism is secondary to increased adrenal stimulation by aldosterone-stimulating factor, we measured the latter in seven patients with idiopathic hyperaldosteronism and in four patients who had undergone surgical removal of an aldosterone-producing adenoma [1].
• Sixteen patients had severe hypokalemia, hyperaldosteronism, and elevated plasma levels of 18-hydroxycorticosterone suggestive of an adenoma [2].
• Glucocorticoid-remediable aldosteronism (GRA), an autosomal dominant disorder, is characterized by hypertension with variable hyperaldosteronism and by high levels of the abnormal adrenal steroids 18-oxocortisol and 18-hydroxycortisol, which are all under control of adrenocorticotropic hormone and suppressible by glucocorticoids [3].
• A patient with hypokalemic alkalosis, normotensive hyperreninism, hyperaldosteronism, increased levels of urinary and plasma prostaglandin E, and vascular hyporesponsivity to angiotensin II was thought to have Bartter's syndrome [4].
• The importance of K for the hyperaldosteronism during dietary Na restriction was verified by the observation that superimposition of K restriction led to hypotension in Agt+/+ and uniform death in Agt-/- mice along with a reduction in P(aldo) by 75 and 90%, respectively [5].

High impact information on Hyperaldosteronism

• In the patients with hyperaldosteronism, plasma aldosterone concentrations (mean +/- 1 S.E.) were 38 +/- 10 and 78 +/- 19 ng per deciliter in the supine and upright position, respectively (P less than 0.01) [1].
• Hazards of long-term dexamethasone treatment in primary aldosteronism [6].
• A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension [3].
• This results in aldosterone biosynthesis being regulated by ACTH, a condition termed glucocorticoid-suppressible hyperaldosteronism [7].
• Landmark perspective: Renin in aldosteronism. Relating kidney and adrenal [8].

Chemical compound and disease context of Hyperaldosteronism

• Captopril prevented and reversed the secondary hyperaldosteronism and hypokalaemia induced by simultaneous diuretic administration, thus eliminating the need for potassium supplements [9].
• In patients with primary hyperaldosteronism adrenal-vein plasma aldosterone/cortisol concentration ratios successfully lateralised all 21 adenomas [10].
• The absorptive mechanisms of K+ are not disturbed by diarrhea per se, but fecal K+ losses are increased in diarrheal diseases by unabsorbed anions (which obligate K+), by electrochemical gradients secondary to active chloride secretion, and probably by secondary hyperaldosteronism [11].
• Metoclopramide and secondary hyperaldosteronism [12].
• We have compared four localizing techniques--adrenal venography, adrenal isotopic scanning, a modified adrenal venous sampling for steroid measurements, and the anomalous postural decrease in plasma aldosterone concentration--in 51 patients with primary aldosteronism, all of whom had undergone operative confirmation [13].
• Genetic studies excluded mutation at the aldosterone synthase locus, further distinguishing this disorder from glucocorticoid-remediable aldosteronism [14].

Biological context of Hyperaldosteronism

• Glucocorticoid-suppressible hyperaldosteronism is a dominantly inherited form of hypertension believed to be caused by the presence of a hybrid CYP11B1/CYP11B2 gene which has arisen from an unequal crossing over between the two CYP11B genes in a previous meiosis [15].
• DESIGN: Retrospective analysis of the following data from 82 patients with primary aldosteronism: blood pressure, serum electrolytes, urinary aldosterone and electrolytes, computed tomographic scans, plasma renin and aldosterone before and during upright posture, atrial natriuretic peptide, and adrenal vein aldosterone and cortisol [16].
• The effect of metoclopramide and domperidone, two dopamine antagonists, administered to cirrhotic patients with ascites and secondary hyperaldosteronism, was examined to evaluate the changes in plasma aldosterone levels and in spironolactone-induced diuresis [17].
• Plasma renin activity and blood volume in uncontrolled diabetes. Ketoacidosis, a state of secondary aldosteronism [18].
• The presence of increased plasma renin activity and increased urinary aldosterone suggest that in this patient the occurrence of the edema after she discontinued use of the laxative was due to secondary aldosteronism presumably caused by plasma volume depletion [19].

Anatomical context of Hyperaldosteronism

• Moreover, the induction of amiloride-sensitive Isc by secondary hyperaldosteronism was inhibited in hypothyroid adult rats, and the effect of thyroid hormones on amiloride-sensitive Isc could not be explained by changes in the plasma aldosterone concentration [20].
• Furthermore, the level of ANP mRNA in the adrenal glands of patients with primary aldosteronism was obviously elevated compared to that in the kidney donors [21].
• Persistent hyperaldosteronism in the face of a decrease in PRA indicated the development of tertiary hyperaldosteronism due to autonomously functioning zona glomerulosa [22].
• The number of mineralocorticoid-binding sites on mononuclear leukocytes and plasma aldosterone (aldo) concentrations were measured in patients with different types of primary hyperaldosteronism [23].
• Renin-aldosterone response to dexamethasone in glucocorticoid-suppressible hyperaldosteronism is altered by coexistent renal artery stenosis [24].

Gene context of Hyperaldosteronism

• Glucocorticoid-suppressible hyperaldosteronism results from hybrid genes created by unequal crossovers between CYP11B1 and CYP11B2 [25].
• In the same subjects, we sought the chimeric CYP11B1/CYP11B2 that is candidate gene for glucocorticoid-remediable hyperaldosteronism [26].
• The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism [27].
• One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients [27].
• This exacerbated aldosterone production in kcne1(-/-) mice is accompanied by an abnormally high plasma renin concentration, which could partly explain the hyperaldosteronism [28].

Analytical, diagnostic and therapeutic context of Hyperaldosteronism

• Plasma atrial natriuretic peptide in primary aldosteronism (before and after treatment) and in Bartter's and Gordon's syndromes [29].
• It is hypothesized that the hyperaldosteronism attending this model stems from the combination of fixed dietary potassium load in the face of reduced filtration on the one hand, and persistent renin secretion from the scarred remnant kidney on the other [30].
• These results suggest that despite the same severity of myocardial hypertrophy between primary aldosteronism and essential hypertension, the myocardial damage estimated by thallium-201 myocardial scintigraphy is more severe in primary aldosteronism than in essential hypertension [31].
• Single dose captopril as a diagnostic test for primary aldosteronism [32].
• We investigated the effects on the heart of hypertension due to the excess of aldosterone and suppression of the renin-angiotensin system caused by primary aldosteronism with M-mode echocardiography and transmitral Doppler flow velocity measurements [33].

References