|
Antidiuresis |
Diuresis |
What? |
Arginine-vasopressine or antidiuretic hormone |
Angiotensine II |
Aldosterone |
Atrial natriuretic peptie |
Site of synthesis? |
Neurohypophysis |
Lungs |
Adrenal glands |
Atria |
Site of effect in kidney? |
Cortical and medullary collecting tubule |
Proximal tubule |
Cortical collecting tubule (epithelial sodium channels) |
Glomeruli & inner medullary collecting duct |
Receptors? |
V2-receptor |
AT1-receptor |
MR-receptor |
NPR-A |
Main effect in kidney? |
Antidiuresis through water reabsorption by fusion of aquaporin-2 channels with luminal membrane |
Antidiuresis through:
Sodium reabsorption, both directly and indirectly (stimulation of aldosterone secretion)
Water reabsorption, indirectly (sodium reabsorption and stimulation of ADH) |
Antidiuresis through sodium reabsorption |
Natriuresis through:
inhibition of sodium reabsorption directly and indirectly (inhibition of RAAS)
inhibition of water reabsorption indirectly (diminish response to ADH) |
Stimulating factors? |
Hyperosmolality
Hypovolemia
stress e.g. pain
hypoglycemia |
Increase in renin due to:
Low blood volume
Low Na+ concentration in distal tubule
Drop in blood pressure |
Ang II
Plasma K+ concentration
ACTH |
Volume expansion with atrial stretch
Aldosterone escape |
Role in nocturnal polyuria? |
Reduced e.g. in nocturnal enuresis |
Reduced e.g. in hypertension |
Reduced e.g. sleep apnea syndrome |
Increased e.g. in heart failure |
V: Vasopressin; AT: Angiotensin; MR:Mineralocorticoid; NPR:Natriuretic Peptide Receptor; ADH:Antidiuretic Hormone; RAAS: Renin-Angiotensin-Aldosteron System; Ang:Angiotensin; ACTH:Adrenocorticotropic Hormone |