Hydrogen ions aldosterone

Aldosterone decreases urinary sodium excretion by increasing sodium reabsorption in the renal tubules at the expense of potassium and hydrogen ions. Aldosterone also stimulates sodium conservation by the sweat glands and the... 

The main endogenous mineralocorticoid is aldosterone, which is mainly produced by the outer layer of the adrenal medulla, the zonaglomerulosa. Aldostorone, like other steroids, binds to a specific intracellular (nuclear) receptor, the mineralocorticoid receptor (MR). Its main action is to increase sodium reabsotption by an action on the distal tubules in the kidney, which is accompanied by an increased excretion of potassium and hydrogen ions. 

The answer is e. (Hardman, p 708.) Spironolactone is a competitive antagonist of aldosterone that blocks the reabsorption of Na and water from the collecting duct in exchange for K and hydrogen ion retention. Therefore, in the presence of hyperkalemia, spironolactone is contraindicated The administration of each of the other diuretic agents listed results in increased excretion of K. 

Aldosterone and other steroids with mineralocorticoid properties promote the reabsorption of sodium from the distal part of the distal convoluted tubule and from the cortical collecting renal tubules, loosely coupled to the excretion of potassium and hydrogen ion. Sodium reabsorption in the sweat and salivary glands, gastrointestinal mucosa, and across cell membranes in general is also increased. Excessive levels of aldosterone produced by tumors or overdosage with synthetic mineralocorticoids lead to hypokalemia, metabolic alkalosis, increased plasma volume, and hypertension. 

Aldosterone secretion is also stimulated by increased plasma potassium concentration. Potassium is secreted into the urine in exchange for reabsorption of sodium in the distal nephron. Aldosterone also promotes secretion of hydrogen ions from the distal tubule according to the acid-base status of the... 

In the distal tubule (site 4), sodium ions are exchanged for potassium and hydrogen ions. The sodium ions are transported across the epithelial Na chaimel (called ENaC), which is stimulated by aldosterone. The aldosterone (mineralocorticoid)... 

Concurrent acidosis in patients with trimethoprim-induced hyperkalemia is uncommon, which could be explained if the action of trimethoprim, like that of amiloride, is hmited to the cortical collecting tubule but does not affect the medullary collecting tubule, which has a large capacity to secrete hydrogen ions and may therefore prevent the development of acidosis. Predisposing factors for the rare adverse effect of renal tubular acidosis in this case may have been aldosterone deficiency or resistance, medullary dysfunction of sickle cell anemia, and renal insufficiency. All these factors could contribute to impaired renal handling of secretion of hydrogen ions (72). 

Aldosterone acts in the connecting segments and collecting ducts to increase the reabsorption of sodium and chloride ions and promote the excretion of potassium and hydrogen ions. As with all steroid hormones, aldosterone acts by diffusing into the tubular cells and attaching to specific cytosolic receptors. These complexes are... 

Selective Aldosterone Deficiency (Type IV RTA). In type IV RTA, there is failure of distal potassium and hydrogen ion secretion because of aldosterone deficiency or resistance. This may occur because of a range of steroid or steroid receptor synthetic defects or because of hyporeninemic hypoaldosteronism (e.g., due to diabetic nephropathy, tubulointerstitial disease, urinary obstruction, renal transplantation, or SLE). Hyperkalemia, although mild, is a usual manifestation. 

Figure 15-6. Mechanisms of sodium, potassium, and hydrogen ion movement and water reabsorption in the collecting tubule cells. Synthesis of Na+/K+ ATPase and sodium and potassium channels is under the control of aldosterone, which combines with an intracellular receptor, R, before entering the nucleus. ADH acts on its receptor, V, to facilitate the insertion of water channels from storage vesicles into the luminal membrane. (Reproduced, with permission, from Katzung BG [editor] Basic Clinical Pharmacology, 8th ed. McGraw-Hill, 2001.)...

The adrenal cortex secretes a potent mineraiocorticoid called aldosterone, which promotes salt and water retention and potassium and hydrogen ion excretion. 

Conn s disease is primary hyperaldosteronism caused by a rare aldosterone-secreting tumour. Consequently, excessive amounts of potassium and hydrogen ions are lost in the urine resulting in hypoka-laemia and metabolic alkalosis. Secondary hyperaldosteronism due to kidney or liver disease is more common. 

A hormone produced in the adrenal gland, aldosterone, signals the kidneys to excrete or retain potassium based on the body s needs. If potassium levels are high, aldosterone is secreted, causing an increase in potassium excretion into the urine. Serum levels of potassium also are influenced by the levels of other electrolytes and acid-base balance. In alkalosis, for example, potassium may shift out of the cell as hydrogen ions shift into the cell to buffer the excessive acid, and when serum potassium concentration is low, potassium is retained by excreting sodium and chloride. 

From the point of view of potassium balance, there is increased renal excretion of potassium, loss of potassium in the vomitus and no potassium being delivered for absorption in the alimentary tract. All these factors contribute to a severe depletion of the body s total potassium content. Yet another factor contributes to potassium loss. A drop in volume of the circulating blood leads to aldosterone secretion via the renin-angiotensin mechanism which, in turn, promotes sodium reabsorption in the renal tubule this contributes further to excessive renal loss of potassium and hydrogen ions. The acidity of the urine is inappropriate as a response to metabolic alkalosis, but the preservation of electrolyte and fluid volume takes precedence over the acid-base disturbance. These various efiects all combine to yield a positive feedback system driving the metabolic alkalosis which, if not treated, reaches lethal levels in a few days. 

---