Physio 6 Flashcards
why is there an increase in TF/P for Cl-?
reflects the preferential reabsorption of HCO3 rather than Cl- in the early proximal tubule.
why is there a change in transepithelial voltage from -3 to +3?
net efflux and reabsorption of more positively charged cationic solutes in the first 25% of the PT and the net efflux and reabsorption of more negatively charged anionic solutes downstream
proximal tubule Na reabsorption
occurs both paracellularly and transcellularly. mediated by uptake at the apical membrane and efflux at the basal and lateral membrane.
Na+ travels down the electrochem gradient into the cell, and across the basal and lateral membrane against the gradient.
paracellular backleak of Na+
happens in the early PT, approx 33% of the transported Na transcelluarly travels back int othe lumen. in the late PT, the voltage difference reverses, and a Na is driven back into the peritubular space
proximal tubule Cl- reabsorption
paracellular in the early and late PT, transcellular in the late PT.
driven by negative voltage difference in the early PT. due to preferential HCO3 reabsorption in early PT, the Cl concentration is higher than plasma.
in late PT, the efflux of Cl creates positive diffusion potential, which helps push Na through the paracellular pathway
proximal tubule water reabsorption
most of the glomerular filtrate is returned to circulation at the PT where reabsorption of tubular fluid occurs without a change in osmolarity. passive, trans and paracellular. small osmotic gradient due to Na and Cl reabsorption. high leakiness of PT allows a lot of water to move through such a small gradient. movement of watter from lumen to peritubular space is driven by active Na transport dependent increase in osmolarity
role of proximal tubule in acid base homeostasis
reabsorb and return most filtered HCO3 to circulation maintaining a constant HCO3 level in the ECF.
secrete H+ generated from metabolism of amino acids, production of organic acids, intestinal HCO3 loss. secreting H+ generates new HCO3
proximal tubule HCO3 reabsorption
transcellular. coupled to transcellular Na reabsorption. in PT tubular fluid, HCO3 -> CO2 and OH-. H+ is transported out of cell by Na/H antiporter forms H20 with OH-. CO2 goes across luminal membrane and forms HCO3 in cell with OH-.
recycling of H+
transcellular transport process of HCO3 reabsorption does not involve net secretion of H+
saturable induced alkalinization
transcellular transport process mediating HCO3 reabsorption is saturable and increasingly greater amounts of filtered HCO3 will alkalinize the tubular fluid and appear in the urine as HCO3 concentration exceeds a reabsorptive threshold of 40 mM
contraction alkalosis
ECF volume contraction stimulates HCO3 reabsorption due to starling forces increasing PT fluid reabsorption and increased angiotensin II
proximal tubule excretion of H+ as NH4+
protons secreted by PT are also excreted as ammonium. arises from intracellular metabolism of glutamine. NH3 goes to NH4 at cellular pH. for each NH3 -> NH4, a proton is trapped and excreted in the urine and a new HCO3 ion is made inside the PT cell to return to circulation
regulation of PT proton secretion / bicarb synth
renal compensatory response to respiratory acidosis (hypoventilation), a primary increase in ECF Pco2, includes an increase in PT H+ secretion and an associated increase in proximal tubule HCO3 synth. serves to maintain ratio of HCO3 to CO2 to maintain ECF pH. when respiratory alkalosis happens, the reverse of above happens
what does proximal tubule mainly reabsorb
67% of both filtered water as well as filtered NaCl. may increase only when severely volume depleted. reabsorption occurs isosmotically, without a change in NaCl in the 33% of the tubular fluid remaining.
