Evidence from renal proximal tubules that \documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy}\usepackage{mathrsfs}\setlength{\oddsidemargin}{-69pt}\begin{document}\begin{equation*}{\mathrm{HCO}}_{3}^{-}\end{equation*}\end{document} and solute reabsorption are acutely regulated not by pH but by basolateral \documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackag

Zhou, Yuehan; Zhao, Jinhua; Bouyer, Philippe; Boron, Walter F.

doi:10.1073/pnas.0500423102

Cited by 48 publications

(60 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, we observed that increasing levels of basolateral ANG II have a biphasic effect on J HCO 3 . Our J HCO 3 data are consistent with those made by Garvin (19) in rat PSTs Ϫ ] BL at 22 mM and fix pH BL at 7.4, substantially stimulated bicarbonate reabsorption by the rabbit S2 PT (43). In the present study, we examined the effects of low-or high-dose basolateral ANG II on the basolateral CO 2 dependence of J HCO 3 .…”

Section: Effects Of Basolateral Ang II On J Hcosupporting

confidence: 78%

“…The first two were subsequently analyzed for [ 3 H]methoxyinulin for use in the calculation of JV, and the third was analyzed for total CO2 for use in the calculation of JHCO 3 . Our measurement of JHCO 3 (pmol ⅐ min Ϫ1 ⅐ mm Ϫ1 tubule length) and JV (nl ⅐ min Ϫ1 ⅐ mm Ϫ1 ) was similar to that used by McKinney and Burg (28) and identical to our previous approach (41,43). We determined total CO 2 in aliquots of the perfusate and collected fluid using a WPI "NanoFlo" device (World Precision Instruments, Sarasota, FL) together with Diagnostic Kit 132-A (Sigma, St. Louis, MO).…”

Section: Biological Preparationmentioning

confidence: 48%

“…The experimental protocol was similar to that of a previous study (43) except for the addition of ANG II to the luminal or basolateral solutions. Table 1 lists the compositions of the solutions, all of which were identical to those used in the aforementioned study (43). In brief, we dissected PTs in Hanks' solution (solution 1) at 4°C.…”

Section: Biological Preparationmentioning

confidence: 99%

“…In this paper, the values that we report for J HCO 3 (or JV) in first collection period are unnormalized mean values. The values that we report for JHCO 3 (or JV) in the second collection period are normalized, mean values computed as described previously (43). Briefly, in each experiment, we divided the J HCO 3 (or JV) value obtained during the second collection period by the comparable values obtained during the first collection period; the result was a pair of second/first collection-period ratios.…”

Section: Biological Preparationmentioning

confidence: 99%

“…Using out-of-equilibrium (OOE) CO 2 (40,41,43), our laboratory demonstrated that, at least in regard to acute acidbase disturbances, H ϩ secretion by the PT responds not to changes in pH, but only to changes in basolateral [CO 2 ] and [HCO 3 Ϫ ] (43). Thus, in the case of acute respiratory acidosis, the PT cell senses the increase in blood [CO 2 ] per se, which is a powerful stimulus for HCO 3 Ϫ reabsorption.…”

mentioning

confidence: 99%

See 4 more Smart Citations

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Zhou¹,

Bouyer²,

Boron³

2006

American Journal of Physiology-Renal Physiology

Self Cite

View full text Add to dashboard Cite

M tended to reduce stimulation by CO2, and at 10 Ϫ9 M, produced an even greater reduction. In conclusion, the mutual effects of 1) ANG II on the JHCO 3 response to basolateral CO2 and 2) basolateral CO2 on the JHCO 3 responses to ANG II suggest that the signal-transduction pathways for ANG II and basolateral CO2 intersect or merge.kidney; out-of-equilibrium solutions; acid-base; volume reabsorption ONE OF THE MAJOR tasks of the kidneys is to participate, along with the lungs, in the regulation of the acid-base balance of the extracellular fluid. For example, it has long been appreciated that acute respiratory acidosis (i.e., a rise in PCO 2 that causes a fall in pH) rapidly stimulates renal H ϩ secretion (8, 16). The proximal tubule (PT) plays a key role in this acid secretion. In addition to reabsorbing a near-isosmotic fluid that represents about two-thirds of the fluid filtered by the glomerulus, the PT reabsorbs ϳ80% of the filtered HCO 3 Ϫ as follows. The PT cell actively secretes H ϩ into the tubule lumen (1, 6, 35) and uses this H ϩ to titrate filtered HCO 3 Ϫ in the lumen to CO 2 and H 2 O, catalyzed by apical carbonic anhydrase IV (9, 36, 37). The newly formed CO 2 and H 2 O then diffuse into the PT cells, where carbonic anhydrase II (36, 37) catalyzes the regeneration of H ϩ and HCO 3 Ϫ . The cell extrudes the H ϩ across the apical membrane via Na-H exchangers (4, 5, 30) and H ϩ pumps (20), while exporting the HCO 3 Ϫ across the basolateral membrane, mainly via the electrogenic Na/HCO 3 cotransporter (7,15,32,33 (12) on isolated, perfused rabbit PTs. They noted that adding ϳ2 ϫ 10 Ϫ6 M ANG II to the basolateral solution had no detectable effect on the rate of fluid absorption (J V ). In a 1974 rat micropuncture study, Steven (38) reported that ϳ2 ϫ 10 Ϫ5 M basolateral ANG II lowered J V , whereas 1 ϫ 10 Ϫ7 M had no effect. Harris and Young (23) later showed that basolateral ANG II has a biphasic effect on Na ϩ reabsorption in the rat PT, stimulating at low doses (10 Ϫ12 -10 Ϫ10 M) and inhibiting at higher doses (3 ϫ 10 Ϫ7 -3 ϫ 10 Ϫ6 M). Shuster and colleagues (34) in 1984 demonstrated a similar biphasic effect of basolateral ANG II on J V in isolated, perfused rabbit PTs, ruling out a role of sympathetic innervation on the J V response. In 1991, working in isolated, perfused rat proximal straight tubules (PSTs), Garvin (19) found that 10 Ϫ10 M basolateral ANG II increases both J HCO 3 and J V . At about the same time, Chatsudthipong and Chan (14) found that high levels of basolateral ANG II reduce J HCO 3 in rats and that these effects are blocked by saralasin, an antagonist of ANG II receptors.As far as the effects of luminal ANG II are concerned, in a 1988 micropuncture study, Liu and Cogan (26) showed that low-dose luminal ANG II (10 Ϫ12 -10 Ϫ11 M) increases HCO 3 Ϫ reabsorption (J HCO 3 ) even in a denervated rat kidney. The 1990 study on the rat PT by Wang and Chan (39) extended the earlier observations by showing that increasing levels of luminal ANG II have biphasic effects on J HCO 3 as well...

show abstract

Section: Effects Of Basolateral Ang II On J Hcosupporting

confidence: 78%

Section: Biological Preparationmentioning

confidence: 48%

Section: Biological Preparationmentioning

confidence: 99%

Section: Biological Preparationmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Zhou¹,

Bouyer²,

Boron³

2006

American Journal of Physiology-Renal Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

Cation‐Coupled Bicarbonate Transporters

Aalkjær

Boedtkjer

Choi

et al. 2014

Comprehensive Physiology

View full text Add to dashboard Cite

Cation-coupled HCO3− transport was initially identified in the mid-1970s when pioneering studies showed that acid extrusion from cells is stimulated by CO2/HCO3− and associated with Na+ and Cl− movement. The first Na+-coupled bicarbonate transporter (NCBT) was expression-cloned in the late 1990s. There are currently five mammalian NCBTs in the SLC4-family: the electrogenic Na,HCO3-cotransporters NBCe1 and NBCe2 (SLC4A4 and SLC4A5 gene products); the electroneutral Na,HCO3-cotransporter NBCn1 (SLC4A7 gene product); the Na+-driven Cl,HCO3-exchanger NDCBE (SLC4A8 gene product); and NBCn2/NCBE (SLC4A10 gene product), which has been characterized as an electroneutral Na,HCO3-cotransporter or a Na+-driven Cl,HCO3-exchanger. Despite the similarity in amino acid sequence and predicted structure among the NCBTs of the SLC4-family, they exhibit distinct differences in ion dependency, transport function, pharmacological properties, and interactions with other proteins. In epithelia, NCBTs are involved in transcellular movement of acid-base equivalents and intracellular pH control. In nonepithelial tissues, NCBTs contribute to intracellular pH regulation; and hence, they are crucial for diverse tissue functions including neuronal discharge, sensory neuron development, performance of the heart, and vascular tone regulation. The function and expression levels of the NCBTs are generally sensitive to intracellular and systemic pH. Animal models have revealed pathophysiological roles of the transporters in disease states including metabolic acidosis, hypertension, visual defects, and epileptic seizures. Studies are being conducted to understand the physiological consequences of genetic polymorphisms in the SLC4-members, which are associated with cancer, hypertension, and drug addiction. Here, we describe the current knowledge regarding the function, structure, and regulation of the mammalian cation-coupled HCO3− transporters of the SLC4-family.

show abstract

Molecular Mechanisms and Regulation of Urinary Acidification

Kurtz

2014

Comprehensive Physiology

View full text Add to dashboard Cite

The H+ concentration in human blood is kept within very narrow limits, ~ 40 nM, despite the fact that dietary metabolism generates acid and base loads that are added to the systemic circulation throughout the life of mammals. One of the primary functions of the kidney is to maintain the constancy of systemic acid-base chemistry. The kidney has evolved the capacity to regulate blood acidity by performing three key functions: 1) reabsorb HCO3− that is filtered through the glomeruli to prevent its excretion in the urine; 2) generate a sufficient quantity of new HCO3− to compensate for the loss of HCO3− resulting from dietary metabolic H+ loads and loss of HCO3− in the urea cycle; and 3) excrete HCO3− (or metabolizable organic anions) following a systemic base load. The ability of the kidney to perform these functions requires that various cell types throughout the nephron respond to changes in acid-base chemistry by modulating specific ion transport and/or metabolic processes in a coordinated fashion such that the urine and renal vein chemistry is altered appropriately. The purpose of the article is to provide the interested reader with a broad review of a field that began historically ~ 60 years ago with whole animal studies, and has evolved to where we are currently addressing questions related to kidney acid-base regulation at the single protein structure/function level.

show abstract

Cited by 48 publications

References 46 publications

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Cation‐Coupled Bicarbonate Transporters

Molecular Mechanisms and Regulation of Urinary Acidification

Contact Info

Product

Resources

About

Cited by 48 publications

References 46 publications

Effects of angiotensin II on the CO2dependence of HCO3−reabsorption by the rabbit S2 renal proximal tubule

Effects of angiotensin II on the CO2dependence of HCO3−reabsorption by the rabbit S2 renal proximal tubule

Cation‐Coupled Bicarbonate Transporters

Molecular Mechanisms and Regulation of Urinary Acidification

Contact Info

Product

Resources

About

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule

Effects of angiotensin II on the CO₂dependence of HCO₃⁻reabsorption by the rabbit S2 renal proximal tubule