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PubMed1993

Abnormal renal magnesium handling.

The normal fractional urinary excretion of filtered magnesium is about 5%. In magnesium deficiency in man, the kidneys can normally reduce the 24-hour urinary magnesium excretion to less than 1 mmol (24 mg) via unknown mechanisms, and initially without a fall in plasma magnesium concentration. Renal magnesium wasting may be defined as a urinary excretion greater than 1 mmol/day in the presence of hypomagnesemia (plasma magnesium < 0.7 mmol/l). Congenital renal magnesium wasting occurs in several syndromes including Bartter's syndrome in which it is associated with hypercalciuria, and the defect may be in the thick ascending limb of Henle's loop, and Gitelman's syndrome in which there is hypocalciuria, and the defect may be in the distal convoluted tubule. Other causes of renal magnesium wasting include diabetes mellitus, hypercalcemia and diuretics. Magnesium wasting may also result from various toxicities including those of cis-platinum, in which the biochemical features resemble Gitelman's syndrome, and those of aminoglycosides, pentamidine and cyclosporin. Calcitriol deficiency may also contribute to renal magnesium wasting in some circumstances. Mild hypermagnesemia may occur in familial hypocalciuric hypercalcemia and may reflect abnormal sensitivity of the loop of Henle to calcium and magnesium ions. By contrast, the hypermagnesemia that occurs in chronic renal failure results from the reduced glomerular filtration of magnesium.

Animals↗
PubMed1996

[A physiological analysis of kidney ion-regulating function in children with enuresis].

Peculiarities of the excretion of ions (Na, K, Ca, Mg) and water were studied in healthy children and children with the nocturnal enuresis, aged 6-15 years. A greater diuresis in the enuretic children is due to an increased excretion of the osmotically active substances including Na and Mg; excretion of K and Ca does nor differ from the control. A new formula is proposed for the quantitative evaluation of the role of different substances in the osmolar clearance. A high correlation is found between the sodium and magnesium excretion and the osmotic free water reabsorption. A single intranasal administration of 1-deamino-8-D-arginine-vasopressin (DDAVP) to the children before their going to bed returned to the norm the sodium and magnesium excretion in the enuretic children. It is suggested that the defect peculiar to this particular pathology is associated with a decrease in the ion reabsorption in the thick ascending Henle loop. The normal level of the ion transport is restored after stimulation of V2-receptors by DDAVP. An explanation is suggested of the mechanism of the increase of diuresis with a simultaneous rise in the osmotically free water reabsorption in children with enuresis.

Administration, Intranasal↗
PubMed1997

[Diuretics for therapy of patients with hypertension].

Diuretic agents have antihypertensive effects mainly be decreasing extracellular volume and cardiac output. These diuretics are described with regard to mechanism of action, site of action, adverse effects, and drug interactions. Thiazide diuretics inhibit the Na(+)-Cl- symporter in the distal convoluted tubule, by competing for the Cl- binding site, and increase Na+ and Cl- excretion. Loop diuretics are inhibitors of Na(+)-K(+)-2Cl- symporter in the thick ascending limb of the loop of Henle. However, loop diuretics are not the diuretic of first choice and should be reserved for patients in whom other diuretics or antihypertensive drugs do not result in a satisfactory response. The potassium sparing diuretics are used primarily to reduce the kaliuresis and potenciate the hypotensive effect of a thiazide.

Benzothiadiazines↗
PubMed1998

Renal effects of glibenclamide: a micropuncture study.

The renal effects of glibenclamide were investigated using free flow micropuncture techniques in anesthetized Sprague-Dawley rats. Intravenous infusion of the drug (3 mg/hr) evoked a natriuresis and diuresis; potassium excretion remained unchanged. Fractional reabsorption in the proximal convoluted tubule in glibenclamide-infused rats did not differ significantly from that in control animals, although the late proximal tubular fluid to plasma concentration ratio for potassium was reduced. Fractional sodium delivery to the early distal tubule was elevated, while the fractional deliveries of water and potassium to this nephron site were unaffected. We conclude that glibenclamide impairs sodium reabsorption in one or more of the nephron segments that comprise the loop of Henle. These results are consistent with the hypothesis that the natriuresis resulting from glibenclamide administration is a consequence of blockade of potassium channels in the apical membrane of the thick ascending limb of Henle's loop. The data suggest that glibenclamide may additionally inhibit a small secretory potassium flux in the proximal tubule.

Animals↗
PubMed1976

[Renal water-electrolyte excretion and its control mechanisms. Current status of knowledge].

The literature on hydronatriuresis control processes operating at the level of individual renal functional units and of the organ as a whole is analysed. 1) Elementary sodium salt and water tubular transport mechanisms. In converting the filtrate into urine, the kidney expends metabolic energy: this is used in the (active) transport of sodium salts; (passive) transport of water takes place along the osmotic gradients created by salt transfer. The proximal tubules reabsorb the sodium bic-rbonate actively. The reabsorption of the osmitic equivalent of water has the effect of concentrating NaCl in the tubular fluid. An important role in the reabsorption of NaCl is played by passive diffusion from the lumen to the interstitial fluid; the remainder is transferred actively, perhaps by an electrically neutral pump. With respect to the other nephronic segments, the proximal tubule has a relatively high passive permeability to water and salts: active transport here must not surmount high friction resistances nor take place against important concentration gradients. The low permeability of the distal nephron, on the other hand, increases the energy cost of salt transport; for the same reason, important electrochemical gradients are created and the composition of tubular fluid is drastically altered. 2) Elementary mechanisms of tubular potassium transport. Potassium is reabsorbed actively along the whole nephron by a luminal pump. The proximal tubules and Henle loops promote practically complete absorption of filtrated potassium. The distal tubules and collectors have the two-fold capacity of secreting and reabsorbing cation: the quantity of potassium excreted with the urine depends on the degree of excess of the secretion process. At distal tubular level, potassium secretion is a passive phenomenon dependent on the favourable transluminal gradient of the cation's electrochemical potential. 3) Renal function and volume homoeostasis of extracellular fluid. The organism's sodium content is largely controlled by renal excretion of sodium; homoeostasis of the sodium mass guarantees volume homoeostasis of the extracellular fluid through thirst and osmotic secretion of ADH. Extracellular fluid volume errors are picked up by the organism to the extent to which they translate themselves into pressure variations in the low pressure vascular system or into variations in haematic constituent concentration within the vascular sector, produced with velocities independent, at least in the short term, of the volume of extracellular fluid. In control of natriuria are the glomerular filtrate, intrarenal distribution of blood flow and tubular reabsorption of sodium; in its turn, the latter is subject to nervous and hormonal influences and influences from the physical environment surrounding the nephrons...

Aldosterone↗
PubMed1999

[The evolution of osmoregulation in vertebrates (on the centenary of the birth of E. M. Kreps)].

The paper substantiates the point of view that the first step in the evolution of osmoregulation in vertebrates involved development of water-impermeable epithelium which depended on specific distribution of aquaporins in plasma membranes, secretion of autacoids, formation of water-impermeable cell contacts with a high electrical resistance. Migration of vertebrates to the land was associated with appearance of the ability to regulate osmotic permeability of epithelium in a number of organs involving vasotocin and other pituitary hormones, insertion of aquaporins into the luminal plasma membrane. Enhancement of the renal role in the water-salt balance, intensification of the kidney function was due to a rise in renal circulation, glomerular filtration rate, and tubular reabsorption which, despite the increase in the energy expenditure, provided for an obvious enhancement of the renal work efficiency in maintaining the constancy of the internal medium. Colonisation of desert regions became possible in birds and mammals due to development of the system of urine osmotic concentration. Unlike the accepted point of view that this depended on the appearance of Henle's loops, the statement is substantiated that the leading role in this process is played by differentiation of the kidney into the cortex and medulla, as at our Laboratory nephron loops similar to Henle's loop have been revealed in the lamprey. In the vertebrates, the evolution shifted from the polyorgan to mono-organ type of osmotic homeostasis maintenance, with the leading role of the kidney in maintaining physico-chemical constants of the internal medium fluids.

Amino Acid Sequence↗
PubMed1981

[3-Dimensional model of the contribution of the vascular and tubular components of the osmoregulatory apparatus of the kidney].

The method of preparing consecutive series of the reconstruction models of vascular and tubular components of the countercurrent renal system being formed was used to examine their structural organization and spatial interrelations during the prenatal period of rabbit ontogenesis. It was established that the structural and functional unit of the renal osmoregulatory apparatus is represented by a cone-like bundle of tubular formations (the collecting tubule, ascending and descending portions of Henle's loops, vessels) where the central place is occupied by the collecting tubule around which three homogeneous looped tubules of Henle are arranged in a definite manner, the later tubules communicating with the collecting tubule. The presence of the three Henle's loops is accounted for by the fact that each generation of Wolf's duct diverticulum derivatives gives rise to three new populations at whose blind ampullar end there takes place the formation of nephrons.

Animals↗
PubMedDate not supplied

Genotype-phenotype correlations in normotensive patients with primary renal tubular hypokalemic metabolic alkalosis.

Among the different forms of hereditary renal tubulopathies associated with hypokalemia, metabolic alkalosis and normotension, two main types of disorders have been identified: Gitelman disease, which appears to be a homogeneous post-Henle's loop disorder, and Bartter syndrome, a heterogeneous Henle loop disorder. A specific gene has been found responsible for Gitelman disease, encoding the thiazide-sensitive Na-Cl cotransporter (TSC) of the distal convoluted tubule. From a phenotypic point of view the characteristic findings of this disease are hypocalciuria, hypomagnesemia and tetanic crises appearing during childhood or later. Many subjects are asymptomatic. At least three different genes have been shown to be responsible for Bartter syndrome, characterized by mutations in the proteins encoding respectively the bumetanide-sensitive Na-K-2Cl cotransporter, the inwardly-rectifying renal potassium channel and a renal chloride channel, all protein transports located in the ascending limb of Henle's loop. Mutations in the first two transport proteins have been demonstrated in patients with the hypercalciuric forms of Bartter syndrome associated with nephrocalcinosis (respectively Bartter syndrome type I and II), who were often born after pregnancies complicated by polyhydramnios and premature delivery. Mutations in the gene encoding a renal chloride channel were recently recognized in patients with a Henle tubular defect not associated with nephrocalcinosis (Bartter syndrome type III). Most of the latter group of patients were normo-hypercalciuric and presented dehydration and life-threatening hypotension in the first year of life. However, these three genes do not explain all the patients with Bartter syndrome which unlike Gitelman disease, appears to be a very heterogeneous disorder. Clearance studies, especially if done during furosemide and/or hydrochlorothiazide administration, have been helpful in identifying the site of tubular involvement. Considering both phenotypic and genotypic data, we propose a clinical-pathophysiological and molecular approach to diagnose the different tubulopathies associated with hypokalemic metabolic alkalosis.

Alkalosis↗
PubMed1976

Intrarenal blood flow distribution in the desert quail following salt loading.

The total-kidney glomerular filtration rate (GFR) falls when birds are salt loaded. This fall in GFR is caused by glomerular intermittency. The nephrons that stop filtering are small, surface nephrons without loops of Henle. Larger nephrons with loops of Henle in the deeper regions of the kidney continue to filter during salt loading. Microfil casts were made of the renal microvasculature of the desert quail, Lophortyx gambelii, in an attempt to determine at what points intrarenal blood flow is regulated to cause glomerular intermittency. Casts of the renal vasculature were made in quail that were hydrated and in quail that were salt loaded. The results indicate that the small, surface nephrons stop filtering during salt loading because of a vasoconstriction at the level of the afferent arterioles of these nephrons. At the same time, blood flow is maintained to the large nephrons with loops of Henle. Reducing GFR at the expenses of excreting wastes can be viewed as a mechanism to conserve body water during periods of water deprivation.

Adaptation, Physiological↗
PubMed2004

Neuronal nitric oxide synthase inhibition sensitizes the tubuloglomerular feedback mechanism after volume expansion.

BACKGROUND: In the kidney the neuronal isoform of nitric oxide synthase (nNOS) is located in the macula densa cells. These cells are known to be the sensor in the tubuloglomerular feedback. During volume expansion (VE), the tubuloglomerular feedback response is attenuated, allowing increased water and salt excretion. This study addressed the question whether inhibition of nNOS reestablishes the tubuloglomerular feedback response caused by acute extracellular VE. METHODS: In rats, VE was achieved by infusion of isotonic saline solution at 50 mL/hour x kg body weight. When urine flow was stabilized, the tubuloglomerular feedback response was evaluated by measuring changes in proximal tubular stop-flow pressure (PSF) in response to various loop of Henle perfusion rates. The loop of Henle was perfused with artificial ultrafiltrate and with addition of 1 mol/L non-specific NOS inhibitor, Nomega-nitro-l-arginine methyl ester (L-NAME). In additional rats the nNOS inhibitor, 7-nitro indazole (7-NI), was given intraperitoneally. Single nephron glomerular filtration rate (SNGFR) was also measured. GFR was determined after VE and nNOS inhibition. RESULTS: Acute VE decreased DeltaP(SF) and DeltaSNGFR while increasing the turning point, indicating decreased sensitivity of tubuloglomerular feedback response. After administration of L-NAME or 7-NI, DeltaP(SF) was maximally sensitized and the turning point and DeltaSNGFR were restored. GFR decreased after VE and nNOS inhibition compared to that after VE alone. CONCLUSION: These results suggest that a functioning nitric oxide system, especially through the nNOS, is important in mediating normal renal responses and that increased production of and/or sensitivity to nitric oxide during sustained VE plays an important role in the adaptive mechanism of the tubuloglomerular feedback.

Animals↗
PubMed1990

Effect of Na and Cl infusion on loop function and plasma renin activity in rats.

Inhibition of plasma renin activity (PRA) by saline has been shown to be related to a specific effect of chloride. The purpose of this study was to test the hypothesis that inhibition of renin release by selective chloride infusion in the rat is related to increased chloride transport in the thick ascending limb of the loop of Henle (TALH). Measurements of loop of Henle function were obtained by micropuncture before and after a 5% body wt infusion of solutions containing either 0.15 mol/l NaCl, 0.15 mol/l lysine monohydrochloride (LysCl), or 0.15 mol/l Na-assorted anions (NaAA). Both NaCl and LysCl infusion lowered PRA (60.8 +/- 11.9 to 22.6 +/- 3.7 ng angiotensin I (ANG I).ml-1.h-1 and 53.3 +/- 6.8 to 34.5 +/- 4.6 ng ANG I.ml-1.h-1; P less than 0.05), whereas NaAA infusion had no effect on PRA (66.7 +/- 15.1 to 59.1 +/- 12.4 ng ANG I.ml-1.h-1). Analysis of late proximal and early distal fluid showed that chloride transport in the TALH was significantly elevated by infusion in all three groups, and there were no differences among the groups after infusion. Distal chloride concentration increased in the NaCl and LysCl groups (26 +/- 2 to 37 +/- 1 meq/l and 26 +/- 2 to 36 +/- 2 meq/l; P less than 0.05), but distal chloride concentration decreased in the NaAA group (28 +/- 2 to 22 +/- 1 meq/l; P less than 0.05). There was no correlation between PRA and fluid flow rate or chloride delivery to the distal tubule.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1988

Amino acid transport by juxtamedullary nephrons: distal reabsorption and recycling.

Amino acid transport by juxtamedullary (JM) nephrons and its relationship to transport by superficial cortical (SC) nephrons and to function of vasa recta and collecting ducts were examined in vivo and in situ by free-flow micropuncture of Henle's loops, collecting ducts, and vasa recta and by continuous microinfusion of Henle's loops in exposed rat papillae. Fractional deliveries (FDs) of six neutral amino acids, two acidic amino acids, and taurine to tips of Henle's loops of JM nephrons could be substantially below those to early distal loops of SC nephrons, indicating that reabsorption before loop tips could be greater in JM than in SC nephrons. FDs to collecting ducts lower than to JM loop tips suggested reabsorption distal to loop tips. This was confirmed by continuous microinfusion of ascending limbs of Henle's loops. Distal site of reabsorption is unknown, but amino acids may move passively out of the thin ascending limb and be recycled into vasa recta and descending limb. Recycling of amino acids was supported by high FDs to tips of Henle's loops (sometimes greater than 1.0), higher concentrations in ascending than in descending vasa recta at same papilla level, and high mean concentrations in vasa recta.

Amino Acids↗
PubMed1985

Structure of the avian kidney.

The kidneys from 6 domestic fowl were fixed in situ by perfusion from the left ventricle. In the bird there are two types of nephrons. One reptilian-type without Henle's loop and medullary tissue, and one mammalian-type with Henle's loop lying in medullary tissue. Serial sections from kidney tissue embedded in plexiglass or in paraffin were used to study the architecture of eight reconstructed reptilian-type nephrons from different cortical levels. All reconstructed nephrons had four major bends, but particularly in the subcapsular nephrons additional bends parallel to the kidney surface were found. There was no loop of Henle, but before entering the collecting duct the distal tubule usually had a very thin-walled segment. No proximal convoluted part was found in the reptilian-type nephrons. The length of the tubules varied between 3,000 microns and 6,000 microns. In the distal tubule a macula densa segment was found in all nephrons of the reptilian and mammalian type. The capillary network between the inter- and intralobular veins was composed of increasingly larger capillaries towards the intralobular vein. Segments of the distal tubule were indented into these capillaries and completely surrounded by them. In the nephrons of the mammalian type the proximal tubule was found to be convoluted as is usual for mammalian species.

Animals↗
PubMed2000

Role of Na(+)/H(+) exchanger NHE3 in nephron function: micropuncture studies with S3226, an inhibitor of NHE3.

Na(+)/H(+) exchanger NHE3 is expressed in the luminal membrane of proximal tubule and thin and thick ascending limb of Henle's loop. To further define its role, the novel NHE3 inhibitor S3226 was employed in micropuncture experiments in nephrons with superficial glomeruli of anesthetized rats. Microperfusion of proximal convoluted tubule with S3226 revealed a dose-dependent inhibition of reabsorption (IC(50) of 4-5 microM) with a maximum inhibition of 30% for fluid and Na(+). During microperfusion of Henle's loop (last superficial proximal to first superficial distal tubular loop), no effect of S3226 (10 or 30 microM) on the reabsorption of fluid or Na(+) was observed. Finally, S3226 (30 microM) left the tubuloglomerular feedback response unaltered as determined by the fall in proximal tubular stop-flow pressure in response to increasing loop of Henle perfusion rate. These studies indicate that NHE3 significantly contributes to fluid and Na(+) reabsorption in proximal convoluted tubule. NHE3 appears not to significantly contribute to fluid or Na(+) reabsorption in the loop of Henle (including the S3 segment of proximal tubule) or macula densa control of nephron filtration.

Absorption↗
PubMed2005

Impaired urea accumulation in the inner medulla of mice lacking the urea transporter UT-A2.

Urea transporter UT-A2, the major urea transporter of the thin descending limb of the loop of Henle in short loop nephrons, has been implicated in urea recycling in the medulla, thereby producing concentrated urine. To investigate the physiological role of UT-A2 in vivo, we generated UT-A2-selective knockout mice by deleting the UT-A2 promoter. Western analysis, immunohistochemistry, and quantitative reverse transcription-PCR were used to confirm the specific deletion of UT-A2 with preservation of other UT-A transporters. Compared to wild-type mice, differences in the urine outputs of UT-A2(-/-) mice consuming a normal protein diet (20% protein) were not observed under normal conditions or with dehydration. Likewise, impairment of urea accumulation in the inner medulla of UT-A2(-/-) mice was not observed. On a low-protein diet (4% protein), however, significantly reduced maximal urine osmolality was observed in dehydrated UT-A2(-/-) mice compared to wild-type littermates (2,500 mosmol versus 3,450 mosmol, respectively). A significant reduction in urea accumulation in the inner medulla was also observed in UT-A2(-/-) mice; however, differences in Na(+) and Cl(-) accumulation were not observed. Thus, UT-A2 is important for maintaining a high concentration of urea in the inner medulla when urea supply to the kidney is limited.

Alleles↗