China
Africa
Explore chapters and articles related to this topic
Role of Transport in Chemically-Induced Nephrotoxicity *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
At least 70% of the plasma clearance of GSH is by renal mechanisms. There is significant evidence to indicate the presence of renal GSH conjugate transport. Most of this is related to transport across the basolateral membrane of renal proximal tubular cells. Lash and Jones (1984, 1985) have shown that a sodium-coupled, probenecid-sensitive system is capable of translocating both intact GSH and GSH conjugates across the basolateral membrane. Uptake of S-(1,2-dichlorovinyl-GSH, DCV-GSH) by basolateral membrane vesicles was blocked by GSH, GSSG, and α-glutamylglutamate. The cysteine conjugate (DCV-Cys) did not inhibit transport of DCV-GSH, suggesting the necessity for the presence of the α-glutamyl moiety. Abbott et al. (1984) suggested a second mechanism, namely, the basolateral degradation of GSH conjugates by γ-glutamyltranspeptidase (GGT) and dipeptidases. The resulting Cys conjugate was subsequently accumulated by the proximal tubular cells.
Tubular Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
In the collecting duct type B cells, chloride moves across the luminal membrane by counter-transport with bicarbonate ions produced from intracellular carbonic acid. This process is dependent on the activity of the basolateral membrane hydrogen-ATPase pump. Chloride leaves the cell through a channel in the basolateral membrane.
Immune function of epithelial cells
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Richard S. Blumberg, Wayne Lencer, Arthur Kaser, Jerrold R. Turner
Many luminal materials, including hydrophilic nutrients, are transported by distinct transport proteins within apical and basolateral domains. Most often, apical transporters take advantage of the steep, electrochemical Na+ gradient (from extracellular to intracellular) to provide the driving force for absorption. The basolateral Na+-K+ATPase that maintains the Na+ gradient and pumps apically transported Na+ ions across the basolateral membrane is, therefore, essential to ongoing nutrient transport. Paracellular recycling of Na+ ions from the lamina propria to the lumen (via the tight junction, as discussed later) is essential, as the diet does not otherwise contain sufficient Na+ to support ongoing apical absorption. Solutes absorbed by apical transmembrane transport proteins cross the basolateral membrane via facilitated transporters that operate in a strictly concentration-dependent manner. This allows the basolateral transport proteins to drive nutrient absorption from the enterocyte cytoplasm toward the bloodstream when nutrients are being actively absorbed but to also operate in the reverse direction in order to bring nutrients into the enterocyte when none are present in the lumen, e.g., during fasting. Whether by vesicles or transmembrane transport proteins, transport of solutes, membranes, and cargo from one side, through the cell to the other side, is termed the “transcellular pathway” and is an energy-dependent process.
Iron metabolism and chronic inflammation in IgA nephropathy
Published in Renal Failure, 2023
Zhang-yu Tian, Zhi Li, Ling Chu, Yan Liu, Jin-rong He, Yu Xin, Ai-mei Li, Hao Zhang
Three regulatory mechanisms are relevant to iron metabolism in the kidney, including the IRE-IRP system, HIF regulatory system and renal reabsorption [11,12,43–48]. Many transport proteins and regulatory pathways involved in cellular iron handling have been identified in the kidney [10,45,47,48]. IRP1 and IRP2 are expressed in the kidney, with IRP1 being more distributed in the proximal tubule [45]. HIF1α is found in renal tubular cells, whereas HIF2α is restricted to renal endothelial cells and interstitial cells [47]. HIF2α promotes erythropoietin production by renal interstitial fibroblasts under hypoxic conditions, which can be inhibited by IRP1 [48]. Cultured human glomerular endothelial cells have been shown to express TfR1, FPN and DMT1 [49]. The basolateral membrane is the site of tubular iron export, and the only iron exporter that has been identified in the kidney tubules is FPN, which is present in the proximal tubules [50].
Physiology of sweat gland function: The roles of sweating and sweat composition in human health
Published in Temperature, 2019
Figure 2(d) shows the mechanism of ion reabsorption according to the modified Ussing leak-pump model. On the apical membrane of the luminal cells passive influx of Na occurs through amiloride-sensitive epithelial Na channels. Active transport of Na across the basolateral membrane of the basal cells occurs via Na-K-ATPase, which is accompanied by passive efflux of K through K channels on the basolateral membrane. The movement of Cl is largely passive via cystic fibrosis membrane channels (CFTR) on both the apical and basolateral membranes [9,34,35]. The two cell layers are thought to be coupled and behave like a syncytium. The sweat duct also reabsorbs bicarbonate, either directly or through hydrogen ion secretion, but the specific mechanism is unknown [5,8,36,37]. The activity of Na-K-ATPase is influenced by the hormonal control of aldosterone [38]. Overall the rate of Na, Cl, and bicarbonate reabsorption is also flow-dependent, such that higher sweating rates are associated with proportionally lower reabsorption rates resulting in higher final sweat electrolyte concentrations [39,40]. This concept will be covered in more detail in the Effect of sweat flow rate section below.
Persistent diarrhoea: current knowledge and novel concepts
Published in Paediatrics and International Child Health, 2019
Robert H. J. Bandsma, Kamran Sadiq, Zulfiqar A. Bhutta
Absorption of sodium and chloride ions forms a fundamental mechanism for absorption of fluids. Transporters of the solute carrier 9 (SLC9) family of sodium–hydrogen exchangers and the SLC26 family of anion exchangers are responsible for this process. Hereafter, these ions can be exported across the basolateral membrane via the Na+/K+ ATPase and potassium chloride co-transporter [17]. In the distal colon specifically, sodium ions can also be absorbed through the heterotrimeric epithelial sodium channel [18]. Bacteria such as campylobacter or their enterotoxins have been shown to inhibit the activity of these transporters, thereby inducing diarrhoea [19–21]. Chloride is also actively secreted via the cystic fibrosis transmembrane conductance regulator chloride channels and calcium-activated chloride channels. In cholera or rotavirus infection, stimulation of active chloride secretion is a direct cause of diarrhoea [22,23]. Specific aetiological and contributing factors are discussed in the following paragraphs.