excretions and osmo
Filtration from the Bowman's capsule to the proximal tubule has an osmolarity of about the same as blood (300 mosm/L).
The osmolarity remains relatively stable as water and salt are reabsorbed in the proximal tubule (located in the cortex).
Osmolarity increases as water moves out of the filtrate in the descending loop of Henle (located in the medulla).
Osmolarity peaks at the apex of the loop (~1200 mosm/L).
Osmolarity decreases as salt leaves the filtrate in the ascending loop of Henle (also in the medulla).
Approximately 100 mosm/L at the distal tubule (cortex).
Osmolarity changes little as the filtrate flows through the distal tubule, which is hypotonic to the interstitial fluids of the cortex.
In the collecting duct, the filtrate passes back through the medulla.
Osmolarity increases as the filtrate loses water (and some urea).
~1200 mosm/L at the bottom (similar to fluid of the medulla).
The remaining filtrate is excreted with a minimal amount of water as urine.
Kidney functions are regulated by three mechanisms:
Antidiuretic hormone (ADH) enhances fluid retention by increasing water permeability of the distal tubule and collecting duct:
Produced by the hypothalamus.
Stored and released from the pituitary gland.
Release is triggered when osmoreceptor cells in the hypothalamus detect increased blood osmolarity from body water loss (>300 mosm/L).
Increases water reabsorption in the distal tubule and collecting duct, resulting in decreased blood osmolarity — leads to reduced stimulation of osmoreceptor cells.
Decreased release of ADH (negative feedback).
Drinking water also reduces blood osmolarity.
Necessary to return osmolarity to normal after water loss.
Drinking large amounts of water causes little ADH to be released, resulting in dilute urine due to minimal reabsorption.
Alcohol inhibits ADH release.
Juxtaglomerular apparatus (JGA) is specialized tissue near the afferent arterioles (blood to glomerulus):
When blood pressure, volume, or Na+ concentration decreases, it responds by releasing the enzyme renin into the blood.
Renin converts angiotensinogen to angiotensin II:
Functions as a hormone to increase blood pressure directly by causing constriction of arterioles and stimulating salt and water reabsorption by the proximal tubule.
Increases blood pressure and volume.
Indirectly stimulates adrenal glands to release aldosterone, promoting salt and water reabsorption by the distal tubule.
Increases blood pressure and volume.
Stimulates thirst centers in the brain, leading to increased drinking.
ADH and the renin-angiotensin-aldosterone system (RAAS) cooperate in maintaining homeostasis:
Similar results, but respond to different needs.
ADH responds to increased blood osmolarity due to low intake or loss of water and does not compensate for the loss of salts and body fluids if osmolarity remains unchanged — for example, in cases of severe diarrhea, where both are lost.
RAAS responds by increasing Na+ reabsorption in such cases.
Atrial natriuretic factor (ANF) opposes RAAS:
Released by the atria of the heart in response to increased blood pressure and volume.