BIPN 100 Lecture 27: BIPN 100 Lecture 27
BIPN 100 Lecture 27
6/8/2018
• Interstitial fluid of the renal cortex is 300 mOsm
• As you go further and further into the medulla, the osmotic gradient increases, from 300
mOsm to 1200 mOsm
• NKCC: sodium-potassium-chloride channel in the ascending loop of Henle
o In the thick segment solutes are reabsorbed, but water cannot follow because
thee’s o auapois
▪ One potassium in, one potassium in, and two chlorides in from the lumen
of the loop of Henle
▪ There are leak channels for K and Cl on the basal side, and the sodium
ATP pump moves the Na out
▪ So then when the filtrate enters the distal tubule, it is hyposmotic
• Similar characteristics in the epithelium of the distal tubule and collecting duct: effected
by hormonal control for water or solute reabsorption
• Vasopressin (aka ADH) has an effect on the distal nephron
o When we need to conserve water, the hypothalamus will produce ADH and is
stored in the PPG. Hypothalamus tells the PPG to release ADH into the
bloodstream, and when it gets to the collecting duct, it binds to vasopressin-2
(V2) receptors. A membrane receptor (cannot cross bilayer) and activates a GS
transduction pathway which activates AC to produce more cAMP, causing an
increase in protein kinase A (PKA), which phosphorylates. It phosphorylates the
storage vesicles where the AQ2 are stored in. The aquaporin is then inserted and
water can be reabsorbed into the interstitial fluid into the peritubular capillaries
• Three stimuli control vasopressin
o High osmolarity causes vasopressin release
▪ There are osmoreceptors in the hypothalamus. If osmolarity goes up
higher than 280 mOsm, the hypothalamus signals PPG to release
vasopressin
o Low BP
o Low blood volume
▪ Generally goes hand in hand with low BP
o
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• Countercurrent exchange
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