High K + intake results in accumulation out-of K + about interstitium of kidney thanks to medullary recycling cleanup. Earlier degree ideal this particular rise in interstitial K + amount would end up in an enthusiastic inhibitory influence on salt transportation inside the newest thicker ascending limb and proximal tubule, which in turn manage lead to enhanced Na + and you will liquids delivery for the distal nephron, permitting increased K + hormonal (6, 53, 54). Because the chatted about below, present research has concerned about just how K + consumption modulates transportation regarding the lowest-capabilities early distal convoluted tubule (DCT) as a way to to switch tubular circulate so you’re able to K + secretory internet sites. This research recommend that the outcome from dietary K + in order to regulate flow and you may delivery regarding Na + so you’re able to K + secretory internet is more regionalized and you may restricted into the lower capacity distal nephron.
The newest resultant upsurge in Na + beginning and you can move plus improved aldosterone facilitates electrogenic K + secretion because of ROMK
The fresh new DCT comprises a great proximal portion (DCT1) and you can a great distal part (DCT2). About DCT1, salt transportation is inspired exclusively by thiazide-sensitive NaCl cotransporter (NCC), whereas for the DCT2, electroneutral NaCl transport coexists that have electrogenic Na + and you may K + transport paths (28). Throughout the DCT2, aldosterone awareness, that is important to facilitate K + homeostasis, initiate and you may gets to this new collecting duct. Cells of your early DCT exert a substantial, albeit indirect, part during the K + hormonal suggested of the fact that changes in transport about very early DCT manage brand new birth off NaCl on the downstream connecting tubule and you may colleting duct, in which the epithelial salt route (ENaC) mediates electrogenic Na + reabsorption and you will in which K + try released (Fig. 3).
Fig. step 3.Older degree (six, 53, 54) has ideal one to repair regarding K + homeostasis from the form regarding high K + dieting intake are set off by an enthusiastic inhibitory aftereffect of K + towards the Na + reabsorption on thicker ascending limb and you can proximal tubule of your kidney, and so facilitating enhanced birth regarding Na + to portions of your distal nephron responsive to mineralocorticoid passion. Previous findings advise that this course of action is more regionalized and you can implicate the brand new distal convoluted tubule (DCT) given that a renal K + sensor. Highest K + intake suppresses electroneutral NaCl transportation on the proximal part of the distal convoluted tubule (DCT1). Aldosterone and you can disperse can also increase K + hormonal through the Maxi-K route. Increased secretion will likely be initiated up on K + entryway with the digestive tract courtesy a keen enteric K + -sensing process you to definitely suppresses Na + -Cl ? cotransporter (NCC) interest from the lack of improvement in plasma amount.
ENaC, epithelial salt channel; Cd, gathering duct
The region of one’s DCT1 instantaneously upstream in the aldosterone-painful and sensitive distal nephron (ASDN) and its particular lower capability characteristics get this phase a more more than likely site getting changes in weight-loss K + intake to help you regulate Na + transport and ensure you to downstream delivery out of Na + is exactly extent needed to ensure repairs away from K + homeostasis without creating adverse effects toward frequency. Dietary intake away from K + , that creates changes in plasma K + amount, contributes to an enthusiastic inhibitory influence on NCC interest. This means that, Na + delivery and you can disperse try increased to the newest aldosterone sensitive and painful K + secretory areas located in the after servings of DCT (DCT2) and you can collecting duct. Meanwhile, the increase within the plasma K + quantity following intake makes aldosterone release on the adrenal gland, which in turn encourages electrogenic K + hormonal owing to ROMK. Each other enhanced circulate and aldosterone stimulate K + hormonal through the Maxi-K route (fifteen, 28).