High K + consumption contributes to buildup out-of K + throughout the interstitium of the renal compliment of medullary recycling. More mature studies advised this particular escalation in interstitial K + concentration create produce an inhibitory influence on sodium transportation within the the latest dense rising limb and you may proximal tubule, which often perform trigger increased Na + and you can liquid birth towards the distal nephron, allowing for enhanced K + hormonal (6, 53, 54). Because the discussed less than, latest research has focused on exactly how K + intake modulates transportation throughout the lower-capacity early distal convoluted tubule (DCT) in an effort to to change tubular circulate so you’re able to K + secretory internet sites. This research advise that the end result out of dietary K + in order to modulate move and you may beginning regarding Na + so you’re able to K + secretory web sites is more regionalized and restricted toward down ability distal nephron.
This new resultant upsurge in Na + beginning and you can disperse and additionally enhanced aldosterone facilitates electrogenic K + secretion through ROMK
The fresh new DCT comprises a great proximal part (DCT1) and you may a distal portion (DCT2). About DCT1, sodium transport try driven solely by thiazide-sensitive and painful NaCl cotransporter (NCC), whereas inside the DCT2, electroneutral NaCl transportation coexists which have electrogenic Na + and you can K + transport paths (28). On the DCT2, aldosterone sensitivity, which is critical to assists K + homeostasis, starts and you may gets to this new meeting duct. Structure of http://www.datingranking.net/jdate-review/ very early DCT use a substantial, albeit indirect, part during the K + hormonal advised because of the proven fact that changes in transportation throughout the very early DCT control the newest beginning out-of NaCl into downstream connecting tubule and you can colleting duct, where epithelial sodium station (ENaC) mediates electrogenic Na + reabsorption and you may where K + is produced (Fig. 3).
Fig. step three.More mature education (6, 53, 54) possess recommended one restoration off K + homeostasis on the function out-of high K + slimming down consumption are brought about by a keen inhibitory aftereffect of K + towards Na + reabsorption regarding heavy ascending limb and you may proximal tubule of the renal, thereby assisting improved delivery off Na + in order to servings of one’s distal nephron responsive to mineralocorticoid passion. Recent observations advise that this step is more regionalized and implicate this new distal convoluted tubule (DCT) since a renal K + alarm. High K + intake prevents electroneutral NaCl transport about proximal portion of the distal convoluted tubule (DCT1). Aldosterone and you will disperse also increase K + hormonal via the Maxi-K route. Increased secretion will be initiated on K + admission towards gastrointestinal tract owing to an enteric K + -feeling method one suppresses Na + -Cl ? cotransporter (NCC) activity about absence of improvement in plasma amount.
ENaC, epithelial sodium channel; Cd, get together duct
The spot of DCT1 instantly upstream on aldosterone-delicate distal nephron (ASDN) and its particular reasonable capability nature get this to phase a far more more than likely website to have changes in diet K + intake so you can modulate Na + transportation and make certain one downstream beginning out of Na + is strictly the total amount wanted to make certain maintenance from K + homeostasis without creating adverse effects on the frequency. Losing weight intake out of K + , that causes changes in plasma K + amount, results in an enthusiastic inhibitory effect on NCC passion. Because of this, Na + beginning and you can circulate try risen up to brand new aldosterone painful and sensitive K + secretory markets found in the later on servings of DCT (DCT2) and you may collecting duct. At the same time, the rise into the plasma K + attention after the intake yields aldosterone launch regarding the adrenal gland, which encourages electrogenic K + secretion compliment of ROMK. One another increased move and you can aldosterone trigger K + secretion through the Maxi-K channel (15, 28).
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