THE PROXIMAL RENAL TUBULAR TRANSPORT OF α-KETOGLUTARIC ACID

1963 ◽  
Vol 41 (1) ◽  
pp. 1099-1104
Author(s):  
P. Vishwakarma
Keyword(s):  
Proximal Tubule ◽  
Physicochemical Characteristics ◽  
Tubular Secretion ◽  
Acid Base Balance ◽  
Concentration Gradients ◽  
Base Balance ◽  
Active Transfer ◽  
Renal Tubular Transport ◽  
Renal Tubular ◽  
Active Reabsorption

The transport of α-ketoglutaric acid along the length of the renal tubule was studied by the stop-flow method in the dog during infusion of sodium α-ketoglutarate. No deliberate attempts to change the acid–base balance were made. Under these conditions this acid was found to be excreted by a combined process of glomerular filtration and tubular reabsorption. This reabsorption was confined only to the proximal tubule. No tubular secretion was seen in any part of the nephron. The concentration gradients between the luminal urine, cell water and the plasma were measured. It was seen that the gradients between the lumen and the cell and between the lumen and the plasma were against the direction of the transport. The gradient between the plasma and the cell was favorable to the uptake of the acid by the cell. Upon consideration of these gradients, the spontaneous pH changes and the physicochemical characteristics of the molecule, the hypothesis was forwarded that an active reabsorption of α-ketoglutarate must occur in the proximal tubule from the lumen into the cell. The possibility of active transfer of this acid from the blood into the cell was also suggested.

THE PROXIMAL RENAL TUBULAR TRANSPORT OF α-KETOGLUTARIC ACID

1963 ◽  
Vol 41 (5) ◽  
pp. 1099-1104 ◽  
Author(s):  
P. Vishwakarma
Keyword(s):  
Proximal Tubule ◽  
Physicochemical Characteristics ◽  
Tubular Secretion ◽  
Acid Base Balance ◽  
Concentration Gradients ◽  
Base Balance ◽  
Active Transfer ◽  
Renal Tubular Transport ◽  
Renal Tubular ◽  
Active Reabsorption

The transport of α-ketoglutaric acid along the length of the renal tubule was studied by the stop-flow method in the dog during infusion of sodium α-ketoglutarate. No deliberate attempts to change the acid–base balance were made. Under these conditions this acid was found to be excreted by a combined process of glomerular filtration and tubular reabsorption. This reabsorption was confined only to the proximal tubule. No tubular secretion was seen in any part of the nephron. The concentration gradients between the luminal urine, cell water and the plasma were measured. It was seen that the gradients between the lumen and the cell and between the lumen and the plasma were against the direction of the transport. The gradient between the plasma and the cell was favorable to the uptake of the acid by the cell. Upon consideration of these gradients, the spontaneous pH changes and the physicochemical characteristics of the molecule, the hypothesis was forwarded that an active reabsorption of α-ketoglutarate must occur in the proximal tubule from the lumen into the cell. The possibility of active transfer of this acid from the blood into the cell was also suggested.

Renal tubular transport of nitrofurantoin

1962 ◽  
Vol 202 (6) ◽  
pp. 1136-1140 ◽  
Author(s):  
James A. Buzard ◽  
Raymond C. Bender ◽  
Esther G. Nohle ◽  
Donald T. Humphrey ◽  
Mary F. Paul
Keyword(s):  
Proximal Tubule ◽  
Transport System ◽  
Weak Acid ◽  
Tubular Secretion ◽  
Acid Transport ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

Tubular secretion of nitrofurantoin has been demonstrated in the dog and the chicken. This secretion has been localized in the proximal tubule and has been shown to be due to the action of the weak acid transport system. Reabsorption of nitrofurantoin by passive, nonionic diffusion has also been illustrated.

AVP-stimulated nucleotide secretion in perfused mouse medullary thick ascending limb and cortical collecting duct

2009 ◽  
Vol 297 (2) ◽  
pp. F341-F349 ◽  
Author(s):  
Elvin Odgaard ◽  
Helle A. Praetorius ◽  
Jens Leipziger
Keyword(s):  
Collecting Duct ◽  
Tubular Secretion ◽  
Hormonal Control ◽  
Similar Response ◽  
Thick Ascending Limb ◽  
Cortical Collecting Duct ◽  
Medullary Thick Ascending Limb ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

Extracellular nucleotides are local, short-lived signaling molecules that inhibit renal tubular transport via both luminal and basolateral P2 receptors. Apparently, the renal epithelium itself is able to release nucleotides. The mechanism and circumstances under which nucleotide release is stimulated remain elusive. Here, we investigate the phenomenon of nucleotide secretion in intact, perfused mouse medullary thick ascending limb (mTAL) and cortical collecting duct (CCD). The nucleotide secretion was monitored by a biosensor adapted to register nucleotides in the tubular outflow. Intracellular Ca2+ concentration ([Ca2+]i) was measured simultaneously in the biosensor cells and the renal tubule with fluo 4. We were able to identify spontaneous tubular nucleotide secretion in resting perfused mTAL. In this preparation, 10 nM AVP and 1-desamino-8-d-arginine vasopressin (dDAVP) induced robust [Ca2+]i oscillations, whereas AVP in the CCD induced large, slow, and transient [Ca2+]i elevations. Importantly, we identify that AVP/dDAVP triggers tubular secretion of nucleotides in the mTAL. After addition of AVP/dDAVP, the biosensor registered bursts of nucleotides in the tubular perfusate, corresponding to a tubular nucleotide concentration of ∼0.2–0.3 μM. A very similar response was observed after AVP stimulation of CCDs. Thus AVP stimulated tubular secretion of nucleotides in a burst-like pattern with peak tubular nucleotide concentrations in the low-micromolar range. We speculate that local nucleotide signaling is an intrinsic feedback element of hormonal control of renal tubular transport.

Renal Tubular Transport of Amino Acids

1971 ◽  
Vol 17 (4) ◽  
pp. 245-266 ◽  
Author(s):  
John Atherton Young ◽  
Benedict Sol Freedman
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Proximal Tubule ◽  
Amino Nitrogen ◽  
High Capacity ◽  
High Specificity ◽  
Brush Borders ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

Abstract Cushny in 1917 first remarked on the extensive amino acid reabsorption which occurs in the nephron. Although many workers since then have studied the nature and localization of the reabsorptive mechanism, progress has been slow because of the technical difficulties of micropuncture work. The bulk of filtered amino nitrogen is reabsorbed in the proximal tubule although the possibility of there being more distal reabsorptive (or secretory) sites cannot be excluded. It is also uncertain whether all segments of the proximal tubule contribute equally to the reabsorptive process. Amino acid reabsorption is an active process involving numerous illdefined steps, the first of which is binding to the brush borders. Renal amino acid transport mechanisms are of two kinds: the high-capacity low-specificity systems transport whole groups of amino acids—the acidic, basic, neutral, and imino-glycine groups—while the other, the low-capacity high-specificity systems, transport single or perhaps pairs of amino acids only.

Histopathological and biochemical evaluations of the kidney inbroiler chickens under acute heat stress conditions.

2017 ◽  
Author(s):  
S.C. Huang ◽  
Y.F. Fu ◽  
Y.F. Lan ◽  
M.U. Rehman ◽  
Z.X. Tong
Keyword(s):  
Heat Stress ◽  
Broiler Chickens ◽  
Serum Markers ◽  
Acid Base Balance ◽  
Tubular Necrosis ◽  
Acute Heat Stress ◽  
Tubular Lumen ◽  
Base Balance ◽  
Histopathological Images ◽  
Renal Tubular

The purpose of the present study was to investigate the correlation between acute heat stress and relevant histopathology and biochemical parameters of kidney function. A total of 80 healthy Arbor Acer (AA) broiler chickens were randomly divided into two groups: CT (Control Temperature; 22±1°C) group and HT (High Temperature; 38±1°C) group. Histopathological images revealed alteration in kidney (renal tubular lumen dilation with tubular necrosis, especially after 10h of heat stress) of broiler chickens in HT group leading to disturbance of acid base balance. Blood urea nitrogen (BUN) and creatinine (CREA) as serum markers of renal dysfunction were elevated significantly (p less than 0.05) after 5h, and especially, after 10h of heat stress (p less than 0.01) as compared with CT group. These results indicated that the evaluation of morphological and functional parameters in kidney is required, in order to monitor broiler chickens exposed to heat stress.

scholarly journals Roles of Renal Proximal Tubule Transport in Acid/Base Balance and Blood Pressure Regulation

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Motonobu Nakamura ◽  
Ayumi Shirai ◽  
Osamu Yamazaki ◽  
Nobuhiko Satoh ◽  
Masashi Suzuki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ang Ii ◽  
Acid Base Balance ◽  
Acid Base ◽  
Blood Pressure Homeostasis ◽  
Base Balance ◽  
Proximal Renal Tubular Acidosis ◽  
Renal Tubular ◽  
Regulation Of Blood Pressure

Sodium-coupled bicarbonate absorption from renal proximal tubules (PTs) plays a pivotal role in the maintenance of systemic acid/base balance. Indeed, mutations in the Na+-HCO3-cotransporter NBCe1, which mediates a majority of bicarbonate exit from PTs, cause severe proximal renal tubular acidosis associated with ocular and other extrarenal abnormalities. Sodium transport in PTs also plays an important role in the regulation of blood pressure. For example, PT transport stimulation by insulin may be involved in the pathogenesis of hypertension associated with insulin resistance. Type 1 angiotensin (Ang) II receptors in PT are critical for blood pressure homeostasis. Paradoxically, the effects of Ang II on PT transport are known to be biphasic. Unlike in other species, however, Ang II is recently shown to dose-dependently stimulate human PT transport via nitric oxide/cGMP/ERK pathway, which may represent a novel therapeutic target in human hypertension. In this paper, we will review the physiological and pathophysiological roles of PT transport.

Role of iNOS and eNOS in modulating proximal tubule transport and acid-base balance

2002 ◽  
Vol 283 (4) ◽  
pp. F658-F662 ◽  
Author(s):  
Tong Wang
Keyword(s):  
Proximal Tubule ◽  
Knockout Mice ◽  
Proximal Tubules ◽  
Wild Type ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Acid Base Status ◽  
Inos Knockout Mice ◽  
Oxide Synthase

Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption ( J v) and HCO[Formula: see text]absorption ( J HCO3) in the proximal tubule and develop metabolic acidosis. The present study examined the transport of fluid and HCO[Formula: see text] in the proximal tubule and acid-base status in mice lacking two other isoforms of NOS, inducible NOS (iNOS) and endothelial NOS (eNOS). Proximal tubules were microperfused in situ in wild-type and NOS knockout mice by methods previously described (Wang T, Yang C-L, Abbiati T, Schultheis PJ, Shull GE, Giebisch G, and Aronson PS. Am J Physiol Renal Physiol 277: F298–F302, 1999). [3H]inulin and total CO2 concentrations were measured in the perfusate and collected fluid, and net J v and J HCO3 were analyzed. These data show that J HCO3 was 35% lower (71.7 ± 6.4 vs. 109.9 ± 7.3 pmol · min−1 · mm−1, n = 13, P < 0.01) and J v was 38% lower (0.95 ± 0.15 vs. 1.54 ± 0.17 nl · min−1 · mm−1, n = 13, P < 0.05) in iNOS knockout mice compared with their wild-type controls. Addition of the iNOS-selective inhibitor l- N 6-(1-iminoethyl) lysine, reduced both J v and J HCO3 significantly in wild-type, but not in iNOS knockout, mice. In contrast, both J HCO3(93.3 ± 7.9 vs. 110.6 ± 6.18 pmol · min−1 · mm−1) and J v (1.56 ± 0.17 vs. 1.55 ± 0.16 nl · min−1 · mm−1) did not change significantly in eNOS knockout mice. These results indicated that iNOS upregulates Na+ and HCO[Formula: see text]transport, whereas eNOS does not directly modulate Na+ and HCO[Formula: see text] transport in the kidney proximal tubules.

Renal Medicine

2019 ◽  
Author(s):  
William White
Keyword(s):  
Vitamin D ◽  
Clinical Medicine ◽  
Collecting Duct ◽  
Objective Structured Clinical Examination ◽  
Junior Doctors ◽  
Acid Base Balance ◽  
Electrolyte Homeostasis ◽  
Base Balance ◽  
Stimulation Of Erythropoiesis ◽  
Renal Tubular

The kidney causes problems for medical students and junior doctors alike— the convoluted journey from plasma to urine, the conundrum of what is reabsorbed and excreted where, and the tangled web of the glomerulonephritides are traditionally learnt, rather than actually understood. As in all clinical medicine, a good place to start is with the fundamen­tals of the organ in question. Passage from plasma to urine follows the pathway: ● Blood ● Glomerulus ● Tubules ● Collecting duct ● Ureter ● Bladder ● Urethra. The primary functions of the kidney are: ● Removal of toxins ● Electrolyte homeostasis ● Maintenance of acid– base balance ● Activation of vitamin D ● Stimulation of erythropoiesis ● Maintenance of blood volume. The challenge then is to implement these basics by being sensitive to deviations from normal physiology: recognizing the accumulation of any potential toxins (hyperkalaemia, uraemia, and acidosis) or the lack of any synthetic products (hypocalcaemia and anaemia), suggesting triggers for such deviations, and pinpointing the specific parts of the anatomy that may be malfunctioning in some way so as to cause impairment. Despite its bad reputation, the kidney reveals more about itself than any other organ and, in theory, should be the easiest to monitor. It achieves this through its raison d’être: urine. Its presence, absence, con­tents, smell, and colour offer a running commentary on the activity of the renal tract at any given point in time— it is the internal, intangible work­ings of specialized cells made physical, measurable, and dippable. So, far from being those much- feared Objective Structured Clinical Examination (OSCE) stations, the dipstick and the catheter are our friends. Or they should be, for it is our ability to harness the information that they pro­vide, allied to the series of numbers on the oft- requested ‘U&Es’ (urea and electrolytes), against a background of wide- ranging symptoms that will make us sensitive to the running of the kidney. This— not just our ability to regurgitate the three types of renal tubular acidosis— is what is at stake in this chapter.

Clinic and diagnosis of metabolic nephropathies in children

1986 ◽  
Vol 67 (5) ◽  
pp. 358-360
Author(s):  
S. V. Maltsev ◽  
V. M. Davydova ◽  
E. I. Zemlyakova
Keyword(s):  
Uric Acid ◽  
Acid Content ◽  
Acid Metabolism ◽  
Calcium Phosphates ◽  
Xanthurenic Acid ◽  
Acid Base Balance ◽  
Residual Nitrogen ◽  
Daily Urine ◽  
Base Balance ◽  
Renal Tubular

We examined 70 patients with metabolic nephropathy (51 with oxaluria predominance, 19 with uric acid metabolism disorders). Distribution of patients into groups was carried out according to the results of multistage research, including analysis of pedigree; repeated biochemical studies, clinical and radiological comparisons. Endogenous creatinine clearance, residual nitrogen level, urea in blood, acid-base balance were determined to characterize the functional state of the kidneys. Renal tubular function was assessed by urinary excretion of calcium, phosphates, amino acids, titratable acids, Zimnitsky's test. To detect metabolic disorders we studied uric acid content in blood and urine, oxalic acid and xanthurenic acid content in daily urine.

Renal Tubular Acidosis in Children Treated With Trimethoprim-Sulfamethoxazole During Therapy for Acute Lymphoid Leukemia

PEDIATRICS ◽  
1992 ◽  
Vol 89 (6) ◽  
pp. 1072-1074
Author(s):  
Jerome Linus Murphy
Keyword(s):  
Renal Tubular Acidosis ◽  
Elevated Serum ◽  
Growth Failure ◽  
Serum Bicarbonate ◽  
Acid Base Balance ◽  
Urine Ph ◽  
Lymphoid Leukemia ◽  
Acute Lymphoid Leukemia ◽  
Base Balance ◽  
Renal Tubular

The antibiotics trimethoprim (TMP) and sulfamethoxazole (SMZ), when used in combination, can cause metabolic acidosis, renal bicarbonate wasting, and growth failure. Retrospective review of repeated random serum chemistries from 10 children receiving TMP-SMZ and maintenance chemotherapy for acute lymphoid leukemia revealed low serum bicarbonate (P = .0002) and elevated serum chloride (P &lt; .0005) concentrations. These values normalized after all medications were discontinued. Prospective study of 8 children receiving TMP-SMZ and chemotherapy for acute lymphoid leukemia revealed lower serum bicarbonate concentrations and higher urine pH following a dose of TMP-SMZ than paired values obtained more than 3 days after a dose. Four children (50%) met serum bicarbonate and urinary pH criteria for the diagnosis of renal tubular acidosis soon after a dose of TMP-SMZ. The occurrence of TMP-SMZ-induced renal tubular acidosis has implications for the acid-base balance of children receiving TMP-SMZ on a long-term basis.

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