Aldosterone release

Adrenal Inhibition of angiotensin II stimulated aldosterone release... 

Hyperkalemia results from reduced angiotensin II-stimulated aldosterone release. The risk of hyperkalemia with ACE... 

A nontrophic hormone acts on nonendocrine target tissues. For example, parathormone released from the parathyroid glands acts on bone tissue to stimulate the release of calcium into the blood. Aldosterone released from the cortical region of the adrenal glands acts on the kidney to stimulate the reabsorption of sodium into the blood. 

Aldosterone released from the adrenal cortex promotes the reabsorption of sodium from the distal tubule and collecting duct. The mechanisms of action of aldosterone include ... 

Renal function can be grossly assessed by hourly measurements of urine output, but estimation of creatinine clearance based on isolated serum creatinine values in critically ill patients may yield erroneous results. Decreased renal perfusion and aldosterone release result in sodium retention and, thus, low urinary sodium (<30 mEq/L). 

Captopril, as well as other ACE inhibitors, is indicated in the treatment of hypertension, congestive heart failure, left ventricular dysfunction after a myocardial infarction, and diabetic nephropathy. In the treatment of essential hypertension, captopril is considered first-choice therapy, either alone or in combination with a thiazide diuretic. Decreases in blood pressure are primarily attributed to decreased total peripheral resistance or afterload. An advantage of combining captopril therapy with a conventional thiazide diuretic is that the thiazide-induced hypokalemia is minimized in the presence of ACE inhibition, since there is a marked decrease in angiotensin Il-induced aldosterone release. 

Vasopressin release has been claimed to be enhanced by metoclopramide, while aldosterone release is impaired (SED-12, 940). 

When salt intake is reduced, a series of "dry look" nemesis arise. Salt contains sodium, and to a lesser degree potassium in the form of potassium iodide. When salt/sodium is reduced or eliminated from the diet the result is increased Aldosterone release. This makes the body excrete more potassium and hold more sodium/water. The resulting water retention gives the athlete a puffy wet look. This is due to electrolyte imbalances. 

In addition to the angiotensin II effects, aldosterone secretion is regulated by increased plasma potassium levels.75,83 Presumably, elevated plasma potassium serves as a stimulus to increase aldosterone release, thus causing increased potassium excretion and a return to normal plasma levels. Finally, there is evidence that ACTH may also play a role in aldosterone release. Although ACTH is primarily involved in controlling glucocorticoid secretion, this hormone may also stimulate mineralocorticoid release to some extent.75... 

The required properties of such an agent Included (1) selectivity for peripheral vascular dopaminergic receptors versus < -and 6-adrenerglc receptors which could mediate pressor and cardiac effects, (2) absence of central dopaminergic and emetic effects, and (3) potent oral renal vasodilator effects. Dopamine has been associated with diuresis and natriuresls. Possible mechanisms include a direct tubular effect on sodium transport, indirect effects produced by changes in total or regional renal blood flow, or effects resulting from a dopamine Induced decrease in aldosterone release from the adrenal (9). Since diuretics play a key role in antihypertensive therapy, the addition of a natriuretic/diuretic component to the renal vasodilator profile would be valuable and appeared to be feasible. 

The 5-HT4 receptors modulate the activities of channels and transporters by increasing cAMP levels. These include activation of L-type Ca2+ channels (326), chloride currents in human jejunal mucosa and rat distal colon (330,331), and the If pacemaker current in atrial myocytes (332) and stimulation of aldosterone release from the adrenal glands (333,334), striatal dopamine release (324), hippocampal and frontal cortex acetylcholine release (335,336), and hippocampal 5-HT release (337). 5-HT4 receptors also inhibit various channels, including a KV3.2-like delayed rectifier K+ channel (303), a voltage-activated K+ channel in colliculi neurons (320,338), a Ca2+-activated, afterhyperpolariz-ing, and K+ current in hippocampus (325). 

Q4 Potassium concentration is mainly controlled by the steroid hormone aldosterone. Aldosterone release from the adrenal cortex can be stimulated by either decreased plasma sodium or by increased plasma potassium concentration. An increase in aldosterone secretion causes retention (reabsorption) of sodium in the distal nephron in exchange for secretion of potassium into the urine. The amount of potassium excreted by the kidney is influenced by the acid-base status of the body. In alkalosis, potassium excretion increases, whereas in acidosis it is decreased. In the distal nephron H+ and K+ compete for excretion in exchange for the reabsorption of sodium. Insulin also affects plasma potassium concentration because it promotes the movement of potassium from the plasma into cells. 

Direct estimation of aldosterone in blood and urine shows a marked rise after injury (Zl). The secretion rate can be measured with a double isotope dilution technique, and increased amounts have been found in the adrenal vein blood and in the urine (Dl, Ul). The pattern of aldosterone release follows that of cortisol and is related in time and extent to changes in sodium and potassium balance and the severity of the injury (C5). 

It was concluded from these and other studies in hypophysectomized animals that ACTH had no effect on aldosterone release. The volume-sensitive renal mechanism appears to be mainly responsible for postoperative aldosterone changes (S4), but it would now appear that ACTH also plays a part in regulating aldosterone secretion (S4). Removal of the pituitary leads to an immediate fall in aldosterone levels in adrenal venous blood (H9). A linear dose response relationship exists between the infusion rate of ACTH and aldosterone secretion rates (H9). Volume receptors in the right atrium and in the vascular tree respond to minor reductions in blood volume and play an important part in stimulating the aldosterone response (Bl, FI). Patients with suppression of cortisol production due to prolonged administration of steroids continue to secrete aldosterone and are able to increase their output after stress indicating the presence of another trophic factor as well as ACTH (T3). 

FIGURE 10.5 Results of a study on rat zona glomcrulosii cells. The effect of angiotensin II w as measured as the amount of aldosterone released into the medium by the cells. (Redrawn with permission from Braley ei a ., 1989.)... 

W Increased aldosterone release Potentiation of sympathetic activity... 

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