Aldosterone-producing adrenal tumor

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. 

Primary aldosteronism usually results from the excessive production of aldosterone by an adrenal adenoma. However, it may also result from abnormal secretion by hyperplastic glands or from a malignant tumor. The clinical findings of hypertension, weakness, and tetany are related to the continued renal loss of potassium, which leads to hypokalemia, alkalosis, and elevation of serum sodium concentrations. This syndrome can also be produced in disorders of adrenal steroid biosynthesis by excessive secretion of deoxycorticosterone, corticosterone, or 18-hydroxycorticosterone—all compounds with inherent mineralocorticoid activity. 

Hyperplasia or tumors of the adrenal cortex that produce excess aldosterone result in a condition known as primary aldosteronism, which is characterized by enhanced sodium and water retention, resulting in hypertension. 

Relatedly, malfunction of one of the sodium-water control mechanisms, such as a kidney that normally excretes excess water, can result in fluid retention and dilutional hyponatremia. The pituitary gland and hypothalamus function to release ADH (which controls water reabsorption), and the cortex of the adrenal gland seaetes aldosterone (which controls sodium reabsorption). An alteration in the function of either of these hormone systems will alter the body s regulation of sodium or water and can result in hyponatremia. 2 For example, in the syndrome of inappropriate antidiuretic hormone (SIADH), excessive ADH is produced (usually by a tumor or some pulmonary diseases such as tuberculosis or bacterial pneumonia), and the kidneys reabsorb excessive fluids, resulting in dilutional hyponatremia. Conditions causing decreased aldosterone secretion include... 

Shull et al. (1956b) draw the conclusion that the striking increase in G-6-Pase activity per gm. of liver observed in tumor-bearing mice indicates that the activity of this enzyme in vivo is probably controlled, at least in part, by the adrenal cortical hormones. The authors also noted that these tumor-bearing mice excrete 0.5 mS- per day total neutral Cjx steroids in the urine of which corticosterone comprised 0.3 ng. (Schull et al, 1956b). Only traces of Compounds E and F and no aldosterone were found. Therefore, the 45 % increase in G-6-Pase activity observed in the tumor-bearing mice was probably produced largely by corticosterone. 

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