Question

Retention of sodium ions and wated bu kidney are affected by glucocorticoids?

a-true

b-false

Answer 1

True

The major effect of mineralocorticoids is the regulation of electrolyte excretion in the kidney. Aldosterone treatment results in increased sodium reabsorption and an increase in excretion of potassium and hydrogen in the renal tubule. Similar effects on cation transport in most other tissues account for all the systemic activity of mineralocorticoids. The primary features of mineralocorticoid excess are positive sodium balance, increased extracellular fluid volume, normal or slightly high plasma sodium, hypokalemia, and alkalosis. Hypocorticism results in renal loss of sodium, hyponatremia, hyperkalemia, and a decrease in extracellular fluid volume and cellular hydration. The 1% decrease in sodium reabsorption that occurs in hypocorticism is enough to cause profound cardiovascular changes, resulting in circulatory collapse, renal failure, and, ultimately, death. Aldosterone modulates sodium levels by activating mineralocorticoid receptors in the distal tubules of the kidney, leading to increased permeability of the apical membrane of the cells lining the cortical collecting tube. However, there is also evidence for a rapid (within minutes) upregulation of sodium-hydrogen exchange by aldosterone that is independent of traditional mineralocorticoid receptors. Aldosterone also increases the activity of the sodium/potassium-adenosine triphosphatase (ATPase) in the serosal membrane. These changes increase sodium reabsorption and generate a higher negative potential in the lumen, which is the driving force for increased potassium and hydrogen excretion. Mineralocorticoids also increase calcium and magnesium excretion, probably due to volume expansion. Prolonged aldosterone treatment results in sodium “escaping,” a cessation of sodium changes, while potassium and hydrogen loss continues to occur. The mechanism for this effect is unknown but may involve mineralocorticoid receptor downregulation and subsequent cessation of hormonal responsiveness.

Glucocorticoid effects on the kidney differ from mineralocorticoid effects. Glucocorticoids increase water diuresis, glomerular filtration rate, and renal plasma flow. Although increases in sodium retention and potassium excretion occur with cortisol, there seems to be no increase in hydrogen excretion. The major renal complications of glucocorticoid therapy are nephrocalcinosis, nephrolithiasis, and increased stone formation as a result of increased urinary calcium and uric acid.

Electrolyte changes also occur outside the kidney in response to mineralocorticoid treatment, in the gastrointestinal mucosa, salivary and sweat glands, and exocrine pancreas. In these tissues, a longer onset period is required to detect significant responses to aldosterone, and no sodium “escape” occurs after prolonged hormone administration. In the intestine, aldosterone does not cause changes in intestinal electrolyte absorption, but glucocorticoids increase sodium and water absorption and potassium secretion. Both glucocorticoid and mineralocorticoid receptors are present in the mucosa, but dexamethasone can bind to both receptor types whereas aldosterone can only bind to its own receptor. Cortisol also increases gastric acid secretion and blood flow to the gastric mucosa, while decreasing the rate of gastric cell proliferation. High doses of glucocorticoids may cause peptic ulceration or aggravate preexisting ulcers.