Large K + intake leads to accumulation out of K + throughout the interstitium of your renal due to medullary recycling. Elderly training advised this particular upsurge in interstitial K + attention carry out end up in an inhibitory influence on salt transport inside the fresh new thick ascending limb and you can proximal tubule, which perform end up in improved Na + and liquid beginning on distal nephron, permitting improved K + hormonal (6, 53, 54). As talked about lower than, latest research has worried about exactly how K + intake modulates transportation from the lowest-ability early distal convoluted tubule (DCT) in an effort to to alter tubular move so you’re able to K + secretory internet sites. These studies suggest that the effect off weightloss K + so you can modulate circulate and beginning away from Na + so you can K + secretory web sites is more regionalized feeld and you may restricted on the all the way down strength distal nephron.
The new resultant increase in Na + birth and you can circulate and enhanced aldosterone encourages electrogenic K + secretion because of ROMK
The fresh new DCT comprises a good proximal portion (DCT1) and you may good distal portion (DCT2). On the DCT1, salt transportation try inspired entirely because of the thiazide-painful and sensitive NaCl cotransporter (NCC), whereas into the DCT2, electroneutral NaCl transportation coexists which have electrogenic Na + and K + transportation pathways (28). Regarding the DCT2, aldosterone susceptibility, that is important to assists K + homeostasis, begins and you may reaches the fresh new meeting duct. Cells of the early DCT exert a substantial, albeit secondary, part when you look at the K + secretion recommended from the simple fact that alterations in transport on very early DCT manage brand new beginning of NaCl towards downstream linking tubule and you can colleting duct, where in fact the epithelial salt channel (ENaC) mediates electrogenic Na + reabsorption and where K + is actually secreted (Fig. 3).
Fig. step three.More mature degree (6, 53, 54) has recommended you to fix out of K + homeostasis throughout the setting of high K + weight loss consumption are triggered by an inhibitory effectation of K + to your Na + reabsorption from the dense ascending limb and proximal tubule of kidney, and therefore facilitating improved delivery out-of Na + in order to portions of the distal nephron tuned in to mineralocorticoid craft. Recent observations advise that this step is far more regionalized and implicate the distal convoluted tubule (DCT) as a kidney K + detector. Highest K + intake suppresses electroneutral NaCl transport on the proximal portion of the distal convoluted tubule (DCT1). Aldosterone and you will circulate can also increase K + secretion through the Maxi-K station. Improved secretion are started abreast of K + entryway toward digestion courtesy an enthusiastic enteric K + -sensing method one to suppresses Na + -Cl ? cotransporter (NCC) craft on the absence of change in plasma amount.
ENaC, epithelial salt station; Cd, meeting duct
The region of the DCT1 instantly upstream on aldosterone-painful and sensitive distal nephron (ASDN) as well as lowest skill characteristics get this to part a more most likely site to have changes in weight-loss K + consumption to modulate Na + transportation and make certain that downstream beginning from Na + is precisely the amount must make certain repair out of K + homeostasis without producing side effects towards regularity. Dieting intake off K + , that causes changes in plasma K + focus, leads to an enthusiastic inhibitory influence on NCC hobby. This means that, Na + delivery and you can move was increased to the fresh new aldosterone sensitive and painful K + secretory segments found in the later on servings of DCT (DCT2) and you may collecting duct. Meanwhile, the increase when you look at the plasma K + amount after the consumption yields aldosterone discharge regarding the adrenal gland, which often facilitates electrogenic K + secretion courtesy ROMK. Both enhanced move and you can aldosterone trigger K + hormonal through the Maxi-K route (15, 28).
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