High K + intake results in buildup of K + from the interstitium of your kidney as a result of medullary recycling. More mature degree ideal this increase in interstitial K + amount perform cause a keen inhibitory effect on salt transport in the new thicker ascending limb and you will proximal tubule, which often would bring about improved Na + and you can liquids birth towards distal nephron, allowing for increased K + hormonal (6, 53, 54). Due to the fact chatted about below, current studies have worried about exactly how K + intake modulates transport on lowest-strength early distal convoluted tubule (DCT) in order to adjust tubular flow to K + secretory websites. These studies recommend that the result out-of weight minichat profile search reduction K + to help you regulate flow and you will delivery of Na + so you’re able to K + secretory internet is more regionalized and you may restricted toward down skill distal nephron.
The newest resultant escalation in Na + delivery and you can disperse and increased aldosterone encourages electrogenic K + hormonal because of ROMK
Brand new DCT constitutes a great proximal section (DCT1) and you may a great distal part (DCT2). Regarding DCT1, salt transportation are driven only by the thiazide-sensitive and painful NaCl cotransporter (NCC), while into the DCT2, electroneutral NaCl transportation coexists that have electrogenic Na + and you will K + transportation routes (28). From the DCT2, aldosterone sensitivity, which is critical to assists K + homeostasis, initiate and you can extends to the brand new gathering duct. Structure of your very early DCT exert a substantial, albeit indirect, character for the K + secretion recommended by the fact that changes in transport about very early DCT control the new beginning out of NaCl towards downstream linking tubule and you can colleting duct, where the epithelial salt channel (ENaC) mediates electrogenic Na + reabsorption and you can where K + was released (Fig. 3).
Fig. step three.Older training (six, 53, 54) keeps ideal you to definitely fix out of K + homeostasis throughout the means off large K + dietary consumption is set off by a keen inhibitory effect of K + towards Na + reabsorption in the thick rising limb and you can proximal tubule of your own kidney, thereby assisting improved beginning out-of Na + so you can portions of one’s distal nephron tuned in to mineralocorticoid craft. Present findings advise that this course of action is much more regionalized and you will implicate brand new distal convoluted tubule (DCT) as a kidney K + alarm. High K + intake inhibits electroneutral NaCl transport on proximal part of the distal convoluted tubule (DCT1). Aldosterone and you can move also increase K + hormonal via the Maxi-K channel. Improved secretion are initiated up on K + entryway toward gastrointestinal tract by way of a keen enteric K + -sensing method you to suppresses Na + -Cl ? cotransporter (NCC) activity throughout the lack of improvement in plasma focus.
ENaC, epithelial sodium station; Cd, gathering duct
The location of your own DCT1 instantly upstream throughout the aldosterone-sensitive distal nephron (ASDN) and its own lower ability character get this to phase a most likely website for changes in dieting K + consumption to help you regulate Na + transport and make certain you to downstream delivery out-of Na + is precisely the quantity must be sure repair of K + homeostasis without causing unwanted effects into frequency. Weightloss consumption out-of K + , that creates alterations in plasma K + amount, leads to an inhibitory influence on NCC activity. As a result, Na + birth and you can disperse are risen up to the new aldosterone delicate K + secretory avenues located in the afterwards portions of the DCT (DCT2) and get together duct. Meanwhile, the rise into the plasma K + focus adopting the consumption creates aldosterone discharge regarding adrenal gland, which facilitates electrogenic K + hormonal because of ROMK. Both improved disperse and you can aldosterone stimulate K + hormonal from Maxi-K channel (15, 28).