Aldosterone-Regulated Sodium Transport and Blood Pressure

Abstract

Aldosterone is a major mineralocorticoid steroid hormone secreted by glomerulosa cells in the adrenal cortex. It regulates a variety of physiological responses including those to oxidative stress, inflammation, fluid disruption, and abnormal blood pressure through its actions on various tissues including the kidney, heart, and the central nervous system. Aldosterone synthesis is primarily regulated by angiotensin II, K+ concentration, and adrenocorticotrophic hormone. Elevated serum aldosterone levels increase blood pressure largely by increasing Na+ re-absorption in the kidney through regulating transcription and activity of the epithelial sodium channel (ENaC). This review focuses on the signaling pathways involved in aldosterone synthesis and its effects on Na+ reabsorption through ENaC.

Reproductive Consequences of Electrolyte Disturbances in Domestic Animals

“…Aldosterone synthesis is also influenced to a lesser extent by the adrenocortical hormone (ACTH) secreted from the anterior pituitary gland. The site of action of aldosterone is in the convoluted distal tubules of the kidneys and the collecting ducts of the nephrons [ 10 , 34 ]. Aldosterone influences sodium and water re-absorption and the excretion of potassium and hydrogen ions by the cells of the distal and collecting ducts.…”

“…Aldosterone influences sodium and water re-absorption and the excretion of potassium and hydrogen ions by the cells of the distal and collecting ducts. Re-absorption of sodium and water is considered to be the main mechanism of increasing blood pressure [ 34 , 35 ].…”

Controls of Central and Peripheral Blood Pressure and Hemorrhagic/Hypovolemic Shock

“…Moreover, Ang II can bind to AT1 receptors on juxtaglomerular cells and inhibits renin production by negative feedback mechanism [95]. Aldosterone is a steroid hormone produced in the mitochondria of cells in a distinct region of the adrenal cortex; zona glomerulosa [96]. Aldosterone is normally released at the basal level; however, in presence of signals from regulatory hormones its release rate is enhanced or inhibited.…”

“…Aldosterone is normally released at the basal level; however, in presence of signals from regulatory hormones its release rate is enhanced or inhibited. Ang II and high serum potassium are major aldosterone release stimuli [96]. Ang II binding to AT1 receptors on zona glomerulosa cells induces closure of potassium channels, which results in favoring the flow of ions that depolarize the membrane and causes opening of voltagegated calcium channels.…”

“…Aldosterone involves multiple activities such as promoting sodium retention and inhibition of potassium retention by the kidneys, and the stimulation of sodium uptake by the colon. In the kidneys, it increases the reuptake of sodium in the thick ascending limb of the loop of Henle, in the distal convoluted tubule, and in the collecting duct by upregulating amiloride-sensitive sodium channels, the sodium-potassium-chloride cotransporter 2 (NKCC2) [96]. Amiloride-sensitive sodium channels assists the passive movement of sodium along its concentration gradient, while NKCC2 uses concentration gradient of sodium to transport sodium, potassium, and chloride from the filtrate into epithelial tubule cells exposed to the lumen of the nephron [100].…”