Autoradiographic study of Diodrast-I131 transport in Necturus kidney

1960 ◽  
Vol 199 (5) ◽  
pp. 931-941 ◽  
Author(s):  
William B. Kinter ◽  
Lucian L. Leape ◽  
Jordan J. Cohen

Renal tubular transport of Diodrast-I131 was studied in Necturus by newly devised autoradiographic methods used in conjuction with classical clearance methods. Clearance measurements on individual animals indicate different types of over-all tubular transport ranging from secretion into tubular urine, heretofore reported in many species, to reabsorption out of tubular urine, so far reported only in Necturus. Diodrast content of tubular urine as disclosed by autoradiography both corroborates clearance data and provides evidence that proximal tubules are the major site of Diodrast transport irrespective of direction. This view is supported by inulin-C14 autoradiographs. In addition, significant amounts of Diodrast were accumulated within proximal tubular cells during all types of transport. With less than 3 mg Diodrast/100 ml arterial plasma, the estimated intracellular concentration ranged from 2 to 19 times that in plasma. At higher plasma levels, tubular transport was overwhelmed and intracellular concentration no longer exceeded that in plasma. These results support a previously formulated theory of simultaneous, bidirectional movement of Diodrast across tubular cells in Necturus kidney.

1958 ◽  
Vol 192 (2) ◽  
pp. 373-378 ◽  
Author(s):  
K. C. Huang ◽  
N. B. King ◽  
E. Genazzani

In renal cortical slices, methylated xanthine diuretics caused a reduction of PAH uptake to 50–70% of the control values with a slight increase in O2 consumption; xanthine, hypoxanthine, guanine and adenine had little effect. Among the three methylated xanthine derivatives studied, 1,3 dimethylxanthine ethylenediamine (Aminophylline) was found to have more inhibitory effect than the others. This inhibitory effect was a function of the concentration of the compound in the medium and cannot be reversed by addition of glutathione as is the case with mercurial diuretics. The potassium exchange between cells and medium and the glycine conjugation of PABA to PAH by the tubular cells were not significantly affected in the presence of aminophylline. The mechanism of the action is discussed and it is postulated that aminophylline or the other methylated xanthine compounds increase the membrane permeability of renal tubular cells, allowing more PAH to leak out.


1963 ◽  
Vol 205 (2) ◽  
pp. 281-285 ◽  
Author(s):  
P. Vishwakarma ◽  
T. Miller

The renal excretion of citrate and calcium was studied in the dog during the infusion of these substances alone or together by the stop-flow method. Citrate per se was found to be reabsorbed only in the proximal tubular area. This reabsorption occurred against marked concentration gradients. Spontaneous variations in the urine pH from 6.11 to 7.11 units did not affect the reabsorption in any way. Infusion of bicarbonate decreased the capacity of the proximal tubule to lower the citrate concentration but did not alter the general pattern of its transport along the nephron length. Calcium without citrate was actively reabsorbed only in the distal tubule. Calcium when given with citrate, did not affect the pattern of citrate transport along the length of the nephron. Citrate did not affect the distal reabsorption of calcium. However, it did produce a proximal reabsorption of calcium. It was postulated that the proximal reabsorption of citrate is active. The molecular requirement for reabsorption of citric acid is discussed.


1955 ◽  
Vol 33 (1) ◽  
pp. 638-650 ◽  
Author(s):  
James G. Foulks

By means of the infusion of small amounts of sodium sulphate it has been possible to elevate the filtered load of inorganic phosphate to the renal tubule in fasted dogs without the administration of exogenous phosphate. Under these circumstances, the reabsorption of phosphate remains virtually complete, even when filtered loads are reached which result in a substantial phosphaturia when phosphate has been administered. By comparing phosphate reabsorption and excretion in fasted animals, and in animals at various intervals after feeding, the existence of homeostatic adjustments in the renal tubular transport of inorganic phosphate has been demonstrated. The available evidence suggests that the intracellular disposition of phosphate itself may be an important factor in determining the rate of renal tubular phosphate transport at filtered loads in the physiological range. The limitations of the determination of the phosphate "Tm" as a device for studying homeostatic processes have been discussed.


2009 ◽  
Vol 297 (2) ◽  
pp. F341-F349 ◽  
Author(s):  
Elvin Odgaard ◽  
Helle A. Praetorius ◽  
Jens Leipziger

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.


2018 ◽  
Vol 315 (6) ◽  
pp. F1720-F1731 ◽  
Author(s):  
Lung-Chih Li ◽  
Jenq-Lin Yang ◽  
Wen-Chin Lee ◽  
Jin-Bor Chen ◽  
Chien-Te Lee ◽  
...  

High levels of serum free fatty acids (FFAs) and proteinuria have been implicated in the pathogenesis of obesity-related nephropathy. CD36, a class B scavenger receptor, is highly expressed in the renal proximal tubules and mediates FFA uptake. It is not clear whether FFA- and proteinuria-mediated CD36 activation coordinates NLRP3 inflammasomes to induce renal tubular injury and inflammation. In this study, we investigated the roles of CD36 and NLRP3 inflammasomes in FFA-induced renal injury in high-fat diet (HFD)-induced obesity. HFD-fed C57BL/6 mice and palmitate-treated HK2 renal tubular cells were used as in vivo and in vitro models. Immunohistochemical staining showed that CD36, IL-1β, and IL-18 levels increased progressively in the kidneys of HFD-fed mice. Sulfo- N-succinimidyl oleate (SSO), a CD36 inhibitor, attenuated the HFD-induced upregulation of NLRP3, IL-1β, and IL-18 and suppressed the colocalization of NLRP3 and ASC in renal tubular cells. In vitro, SSO abolished the palmitate-induced activation of IL-1β, IL-18, and caspase-1 in HK2 proximal tubular cells. Furthermore, treatment with SSO and the knockdown of caspase-1 expression by siRNA both inhibited palmitate-induced cell death and apoptosis in HK2 cells. Collectively, palmitate causes renal tubular inflammation, cell death, and apoptosis via the CD36/NLRP3/caspase-1 axis, which may explain, at least in part, the mechanism underlying FFA-related renal tubular injury. The blockade of CD36-induced cellular processes is therefore a promising strategy for treating obesity-related nephropathy.


1955 ◽  
Vol 33 (4) ◽  
pp. 638-650 ◽  
Author(s):  
James G. Foulks

By means of the infusion of small amounts of sodium sulphate it has been possible to elevate the filtered load of inorganic phosphate to the renal tubule in fasted dogs without the administration of exogenous phosphate. Under these circumstances, the reabsorption of phosphate remains virtually complete, even when filtered loads are reached which result in a substantial phosphaturia when phosphate has been administered. By comparing phosphate reabsorption and excretion in fasted animals, and in animals at various intervals after feeding, the existence of homeostatic adjustments in the renal tubular transport of inorganic phosphate has been demonstrated. The available evidence suggests that the intracellular disposition of phosphate itself may be an important factor in determining the rate of renal tubular phosphate transport at filtered loads in the physiological range. The limitations of the determination of the phosphate "Tm" as a device for studying homeostatic processes have been discussed.


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