Aldosterone release, stimulation

LOX metabolites also have endocrine effects. 12-HETE stimulates the release of aldosterone from the adrenal cortex and mediates part of the aldosterone release stimulated by angiotensin 11, but not that occurring in response to ACTH. 

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. 

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 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. 

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). 

Retention of potassium with ACE inhibitor therapy can occur and is due to the reduced feedback of angiotensin II to stimulate aldosterone release. Hyperkalemia is most likely to occur in patients with renal insufficiency and in those taking concomitant... 

Perindopril erbumine is an ACE inhibitor that competitively inhibits angiotensin-I-converting enzyme, resulting in prevention of angiotensin I conversion to angiotensin II, a potent vasoconstrictor that also stimulates aldosterone release. Clinical consequences are a decrease in BP, reduced sodium resorption, and potassium retention. It is indicated in the treatment of essential hypertension. 

These drugs reduce aldosterone levels (angiotensin II is a major stimulant of aldosterone release) and cause potassium retention. Potassium accumulation may be marked, especially if the patient has renal impairment, is consuming a high potassium diet, or is taking other drugs that tend to conserve potassium, eg, potassium sparing diuretics. Under these circumstances, potassium concentrations may reach toxic levels. 

B. Effects Angiotensin II is a potent arteriolar vasoconstrictor and stimulant of aldosterone release. All directly incTeases peripheral vascular resistance and, through aldosterone, causes renal sodium retention. All also facilitates the release of norepinephrine from adrenergic nerve endings via presynaptic heteroreceptor action. All of these effects are mediated by the angiotensin AT, receptor, a G, -coupled receptor. 

---