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Steroids are well-known mediators of many different physiological functions. Their best characterized mechanism of action involves interaction with well-defined nuclear receptors and regulation of gene transcription. However, rapid effects of steroids have been reported which are incompatible with their classical long-term/slow effects. Although the concept of membrane-bound receptors for steroids which can transduce their rapid effects has been proposed many years ago, it is only recently that such proteins have been identified and characterized. In this review, we will discuss recent data regarding the rapid action of progesterone mediated by newly characterized membrane-bound receptors belonging to the progestin and adiponectin receptor family.

K+ secretion in the distal nephron has a critical role in K+ homeostasis and is the primary route by which K+ is lost from the body. Renal K+ secretion is enhanced by increases in dietary K+ intake and by increases in tubular flow rate in the distal nephron. This review addresses new and important insights regarding the mechanisms underlying flow‐induced K+ secretion (FIKS). While basal K+ secretion in the distal nephron is mediated by renal outer medullary K+ (ROMK) channels in principal cells (PCs), FIKS is mediated by large conductance, Ca2+/stretch activated K+ (BK) channels in intercalated cells (ICs), a distinct cell type. BK channel activation requires an increase in intracellular Ca2+ concentration ([Ca2+]i), and both PCs and ICs exhibit increases in [Ca2+]i in response to increases in tubular fluid flow rate, associated with an increase in tubular diameter. PIEZO1, a mechanosensitive, nonselective cation channel, is expressed in the basolateral membranes of PCs and ICs, where it functions as a mechanosensor. The loss of flow‐induced [Ca2+]i transients in ICs and BK channel‐mediated FIKS in microperfused collecting ducts isolated from mice with IC‐specific deletion of Piezo1 in the CCD underscores the importance of PIEZO1 in the renal regulation of K+ transport. [ABSTRACT FROM AUTHOR]

A detailed knowledge of the lipid composition of components of nephrons is crucial for understanding physiological processes and the development of kidney diseases. However, the lipidomic composition of kidney tubular segments is unknown. We manually isolated the proximal convoluted tubule (PCT), the cortical thick ascending limb of Henle's loop, and the cortical collecting duct from 5 lean and obese mice and subjected the samples to shotgun lipidomics analysis by high-resolution mass spectrometry acquisition. Across all samples, more than 500 lipid species were identified, quantified, and compared. We observed significant compositional differences among the 3 tubular segments, which serve as true signatures. These intrinsic lipidomic features are associated with a distinct proteomic program that regulates highly specific physiological functions. The distinctive lipidomic features of each of the 3 segments are mostly based on the relative composition of neutral lipids, long-chain polyunsaturated fatty acids, sphingolipids, and ether phospholipids. These features support the hypothesis of a lipotype assigned to specific tubular segments. Obesity profoundly impacts the lipotype of PCT. In conclusion, we present a comprehensive lipidomic analysis of 3 cortical segments of mouse kidney tubules. This valuable resource provides unparalleled detail that enhances our understanding of tubular physiology and the potential impact of pathological conditions. Graphical Abstract [ABSTRACT FROM AUTHOR]

These last years, the growth factor GDF15 has emerged as a key element in many different biological processes. It has been established as being produced in response to many pathological states and is now referred to as a stress-related hormone. Regarding kidney functions, GDF15 has been involved in different pathologies such as chronic kidney disease, diabetic nephropathy, renal cancer, and so on. Interestingly, recent studies also revealed a role of GDF15 in the renal homeostatic mechanisms allowing to maintain constant, as far as possible, the plasma parameters such as pH and K+ values. In this review, we recapitulate the role of GDF15 in physiological and pathological context by focusing our interest on its renal effect. [ABSTRACT FROM AUTHOR]

Consumption of salt (NaCl) and potassium (K+) has been completely modified, switching from a rich-K+/low-NaCl diet in the hunter--gatherer population to the opposite in the modern, westernized population. The ability to conserve K+ is crucial to maintain the plasma K+ concentration in a physiological range when dietary K+ intake is decreased. Moreover, a chronic reduction in the K+ intake is correlated with an increased blood pressure, an effectworsened by a high-Na+ diet. The renal adaptation to a low-K+ diet in order to maintain the plasma K+ level in the normal range is complex and interconnected with the mechanisms of the Na+ balance. In this short review, we will recapitulate the general mechanisms allowing the plasma K+ value to remain in the normal range, when there is a necessity to retain K+ (response to low-K+ diet and adaptation to gestation), by focusing on the processes occurring in the most distal part of the nephron. We will particularly outline the mechanisms of K+ reabsorption and discuss the consequences of its absence on the Na+ transport systems and the regulation of the extracellular compartment volume and blood pressure. [ABSTRACT FROM AUTHOR]

The kidneys, by equilibrating the outputs to the inputs, are essential for maintaining the constant volume, pH, and electrolyte composition of the internal milieu. Inability to do so, either because of internal kidney dysfunction (primary alteration) or because of some external factors (secondary alteration), leads to pathologies of varying severity, leading to modification of these parameters and affecting the functions of other organs. Alterations of the functions of the collecting duct (CD), the most distal part of the nephron, have been extensively studied and have led to a better diagnosis, better management of the related diseases, and the development of therapeutic tools. Thus, dysfunctions of principal cell–specific transporters such as ENaC or AQP2 or its receptors (mineralocorticoid or vasopressin receptors) caused by mutations or by compounds present in the environment (lithium, antibiotics, etc.) have been demonstrated in a variety of syndromes (Liddle, pseudohypoaldosteronism type‐1, diabetes insipidus, etc.) affecting salt, potassium, and water balance. In parallel, studies on specific transporters (H+‐ATPase, anion exchanger 1) in intercalated cells have revealed the mechanisms of related tubulopathies like distal renal distal tubular acidosis or Sjögren syndrome. In this review, we will recapitulate the mechanisms of most of the primary and secondary alteration of the ion transport system of the CD to provide a better understanding of these diseases and highlight how a targeted perturbation may affect many different pathways due to the strong crosstalk and entanglements between the different actors (transporters, cell types). [ABSTRACT FROM AUTHOR]

Human nongastric [H.sup.+][K.sup.+]ATPase: transport properties of ATP1al1 assembled with different [beta]-subunits. Am J Physiol Cell Physiol 283: C305-C314, 2002. First published March 20, 2002; 10.1152/ ajpcell.00590.2001.--To investigate whether nongastric [H.sup.+][K.sup.+]-ATPases transport [Na.sup.+] in exchange for [K.sup.+] and whether different [beta]-isoforms influence their transport properties, we compared the functional properties of the catalytic subunit of human nongastric [H.sup.+]-[K.sup.+]-ATPase, ATP1al1 (AL1), and of the [Na.sup.+]-[K.sup.+]-ATPase [[alpha].sub.1]-subunit [[alpha].sub.1] expressed in Xenopus oocytes, with different [beta]-subunits. Our results show that [beta]HK and [[beta].sub.1]-NK can produce functional AL1/[beta] complexes at the oocyte cell surface that, in contrast [[alpha].sub.1]\[[beta].sub.1] NK and [[alpha.sub.1]]/[beta]HK complexes, exhibit a similar apparent [K.sup.+] affinity. Similar to [Na.sup.+]-[K.sup.+]-ATPase, AL1/[beta] complexes are able to decrease intracellular [Na.sup.+] concentrations in [Na.sub.+]-loaded oocytes, and their [K.sub.+] transport depends on intra- and extracellular [Na.sup.+] concentrations. Finally, controlled trypsinolysis reveals that [beta]-isoforms influence the protease sensitivity of AL1 and [[alpha].sub.1] and that AL1/[beta] complexes, similar to the [Na.sup.+][K.sup.+]-ATPase, can undergo distinct [K.sup.+]-[Na.sup.+]- and ouabain-dependent conformational changes. These results provide new evidence that the human nongastric [H.sup.+]-[K.sup.+]-ATPase interacts with and transports [Na.sup.+] in exchange for [K.sup.+] and that [beta]-isoforms have a distinct effect on the overall structural integrity of AL1 but influence its transport properties less than those of the [Na.sup.+]-[K.sup.+]-ATPase [alpha]-subunit. [X.sup.+]-[K.sup.+]-ATPases; [Na.sup.+] transport; Xenopus oocytes; intersubunit interactions

Research has been conducted on the muscle-specific protein (beta)m which is structurally related to the X,K-ATPase beta subunits. This protein has been expressed in Xenopus oocytes and its biosynthesis and its role as a X,K-ATPase alpha subunit chaperone have been investigated and are discussed.

Research has been conducted on the H,K-ATPase alpha and beta subunits interactions necessary for their maturation. The results of the coexpression of the human H,K-ATPase alpha and Na,K-ATPase alpha1 as well as AL1-alpha1 and alpha1-AL1 chimeras are described.