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
stress e.g. pain
Increase in renin due to:
Low blood volume
Low Na+ concentration in distal tubule
Drop in blood pressure
Ang II
Plasma K+ concentration
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
Table 1: Main antidiuretic and diuretic hormones and characteristics