Topic
Sodium bicarbonate
About: Sodium bicarbonate is a research topic. Over the lifetime, 6040 publications have been published within this topic receiving 98423 citations. The topic is also known as: Sodium Bicarbonate & Monosodium Carbonate.
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TL;DR: It is shown that in hypertensive nephropathy, daily sodium bicarbonate is an effective kidney protective adjunct to blood pressure control along with angiotensin-converting enzyme inhibition.
315 citations
TL;DR: Dietary alkali treatment of metabolic acidosis in CKD that is less severe than that for which KDOQI recommends therapy reduces kidney angiotensin II activity and preserves eGFR.
307 citations
TL;DR: The oft-cited rationale for bicarbonate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly and given the lack of evidence supporting its use, it is found that bic carbonate administration for patients with lactic acidosis cannot condone, regardless of the degree of acidemia.
306 citations
01 Jan 1986
299 citations
TL;DR: Investigation of the mechanism of bicarbonate transport across the peritubular cell membrane in rat kidney proximal tubules in situ found evidence for a sodium-independent transport system of acids or bases which is able to regulate cell pH even in sodium-free solutions.
Abstract: The mechanism of bicarbonate transport across the peritubular cell membrane was investigated in rat kidney proximal tubules in situ by measuring cell pH and cell Na+ activity in response to sudden reduction of peritubular Na+ and/or HCO
3
−
. The following observations were made: 1. sudden peritubular reduction of either ion concentration produced the same transient depolarizing potential response; 2. bicarbonate efflux in response to peritubular reduction of bicarbonate was accompanied by sodium efflux; 3. sodium efflux in response to peritubular sodium removal was accompanied by cell acidification indicating bicarbonate efflux; 4. all aforementioned phenomena were inhibited by SITS (10−3 mol/l) except for a small SITS-independent sodium efflux and depolarization which occurred in response to peritubular sodium removal and was not accompanied by cell pH changes; 5. bicarbonate efflux and accompanying potential changes in response to reduction of peritubular bicarbonate virtually vanished in sodium-free solutions. From these observations we conclude that bicarbonate efflux proceeds as rheogenic sodium-bicarbonate cotransport with a stoichiometry of bicarbonate to sodium greater than 1. The question which of the charged species of the bicarbonate buffer system moves cannot yet be decided. Attempts to determine the stoichiometry from the SITS-inhibitable initial cell depolarization and from the SITS-inhibitable initial fluxes suggest a stoichiometry of 3 HCO
3
−
: 1 Na+. In addition to sodium-dependent bicarbonate flux, evidence was obtained for a sodium-independent transport system of acids or bases which is able to regulate cell pH even in sodium-free solutions.
266 citations