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PubMed1975

The development of various generations of nephrons during postnatal ontogenesis in the rat.

The structural development of individual nephrons has been investigated in the kidneys of young rats by microdissection. Superficial, intercortical and juxtamedullary nephrons in Wistar-Konarovice rats aged 2 to 60 days have been followed. At two and five days of age the superficial nephrons were in an early stage of anatomical development. At this time intercortical and juxtamedullary nephrons were more developed, and basically resembled similar structures in adult animals with the exception that the loops of Henle did not have a thin ascending limb. At ten days of age all three types of nephrons were differentiated with the exception that the intercortical nephrons did not possess a thin ascending limb of Henle's loop. At selected stages of development there appears to be a direct relation between the length of the superficial nephrons and the weight of the kidney. Since individual segments of these nephrons do not grow at the same proportional rate, this relationship does not hold when compared to kidney weight.

Age Factors↗
PubMed1988

Mammalian renal modifications in dry environments.

The literature on the role of the kidney and renal morphological modifications in places of limited water supply is reviewed. The anatomical structures for urine concentration found in animals living in desert or arid environments, although not all occurring in one particular animal, are wide medullae, long loops of Henle, long proximal tubules, long collecting tubules, small renal corpuscles, extension of the renal pelvis, well developed elongated papillae, occurrence of giant vascular bundles, specialized ultrastructure of Henle's loops, epithelial changes in the collecting tubule, zonation of the vasa recta and peculiarity of the arterial supply to the kidney. The renal renin content is moderately high in these species. The renin-angiotensin-aldosterone system is very active, retaining Na+ with water. The urine is concentrated at the expense of other electrolytes. Both the renal blood and urinary flow rates are lower than in species with access to unlimited water supply. The juxtaglomerular apparatus components are topographically intimate for effective tubuloglomerular autoregulation of renal blood flow.

Acclimatization↗
PubMed1983

Carbonic anhydrase in the monkey kidney.

The distribution of carbonic anhydrase in the kidney of the cynomolgus monkey was studied by the histochemical method of Hansson. Glomeruli and Bowman's capsule were inactive. Convoluted proximal tubules showed high enzyme activity at the brush border and the basolateral membranes and the cytoplasm. Straight proximal tubules were less intensely stained. In nephrons with long loops of Henle, the descending thin limb contained weak enzyme activity, whereas the ascending thin limb was inactive. The thick limb of Henle's loop displayed most enzyme activity at the luminal cell border. In distal convoluted tubules enzyme activity was restricted to the basal part of the cells. In the late distal tubule, intercalated cells appeared among the "ordinary" distal cells and contained abundant cytoplasmic enzyme. Many intensely stained intercalated cells were also found in the cortical and outer medullary segments of the collecting duct, intermingled with more weakly stained chief cells. In the inner medullary segment of the collecting duct, enzyme activity gradually disappeared. Many capillaries were clearly stained for enzyme activity. The capillary staining apparently varied with that of the kidney tubules; virtually all capillaries in the cortex, but very few in the inner medulla, were stained. The distribution of carbonic anhydrase in the kidney tubules of the monkey is very similar to that in man and in the rat, but the primate kidney differs from the rat kidney by the presence of capillary enzyme activity. The functional importance of this difference is not clear at present.

Animals↗
PubMed2000

Cycloleucine fluxes during rat vasa recta and loop microinfusions in vivo and loop microperfusions in vitro.

Amino acids are apparently recycled between loops of Henle and vasa recta in rat papilla in vivo. To examine this process in the absence of metabolism, we performed continuous microinfusions of rat renal papillary ascending thin limbs (ATLs) and vasa recta in vivo, and microperflusions of isolated rat renal papillary descending thin limbs (DTLs) and ATLs in vitro using the nonmetabolizable, synthetic, neutral amino acid cycloleucine. Like naturally occurring amino acids, approximately = 25% of radiolabeled cycloleucine microinfused into ATLs in vivo was reabsorbed by a process that was not saturable or inhibitable. Also, like naturally occurring amino acids, approximately = 47% (relative to inulin) of radiolabeled cycloleucine microinfused into ascending vasa recta in vivo was transferred directly into ipsilateral tubular structures (probably DTLs) by a saturable and inhibitable process. In DTLs perfused in vitro, unidirectional bath-to-lumen fluxes (Jbl) tended to exceed unidirectional lumen-to-bath fluxes (Jlb), whereas in ATLs perfused in vitro Jlb tended to exceed Jbl, but the differences were not statistically significant. Moreover, none of the unidirectional fluxes was saturable or inhibitable, an observation compatible with apparent reabsorption from ATLs in vivo but incompatible with apparent movement from vasa recta to DTLs in vivo. These in vitro observations are like those made previously for the naturally occurring neutral amino acid L-alanine. The lack of saturation and inhibition, like the previous data on L-alanine, suggest that transepithelial movement of amino acids in thin limbs of Henle's loop may occur via a paracellular route and that regulation of amino acid movement in vivo may involve vasa recta, not DTLs. They also suggest that cycloleucine is a good nonmetabolizable surrogate for the study of neutral amino acid transport in the kidney.

Alanine↗
PubMed1982

Disorders of urinary concentration and dilution.

A new approach to the classification of disorders of urinary concentration and dilution is recommended based on recent studies of how the kidney elaborates a urine of widely varying osmolality. The capacity to concentrate urine depends on ft, the fractional reabsorption of solute delivered to the loop of Henle; fu, the excretion of solute relative to the sum of solute excretion and solute delivery to Henle's loop; fw, the fraction of solute loss by vascular outflow from the medulla relative to that reabsorbed by the loop; and finally, collecting duct response to antidiuretic hormone (ADH). A decrease in ft or in increased fu or fw will diminish urinary concentrating ability, as will resistance of the tubule to ADH. Conversely, urinary dilution depends on the delivery of sodium and water to the ascending limb; NaCl reabsorption by the ascending limb; and the absence of ADH. A decrease in sodium and water delivery to the ascending limb or in NaCl reabsorption by the ascending limb will impair urinary diluting ability, as will the presence of ADH. The consequences of disorders in urinary concentrating and diluting ability vary widely. In an alert patient with an intact thirst center, there may be no consequence; in a patient unable to communicate thirst or whose thirst center is deranged, the results may be catastrophic. Keeping in mind the kidney's few basic requirements for formation of concentrated or dilute urine may help the physician avoid these potentially serious dislocations of water balance.

Absorption↗
PubMed1981

Selective distal nephron damage during isolated kidney perfusion.

The morphologic characteristics of the isolated perfused rat kidney were examined by light and electron microscopy. Following perfusion for 90 min, the cortex appeared normal except for the development of spaces in glomerular mesangial regions and ultrastructural abnormalities in very few proximal tubular cells. In the medulla, descending limbs of the loops of Henle and Collecting tubules appeared normal. During perfusion, however, even under optimal conditions, consistent and reproducible changes rapidly developed in cells of the thick ascending limb of Henle's loop, more specifically, in cells of the straight portion of the distal tubule in the inner stripe of the outer medulla. The changes became progressively more severe as perfusion continued and ranged from swelling of mitochondria at 15 min to complete cellular disruption by 90 min. Horseradish peroxidase added to the perfusion medium was found in and between damaged cells and in the interstitial tissue adjacent to affected areas. The pathogenesis of these selective medullary distal tubular abnormalities may relate to the specialized functional activity of this segment of the nephron. Such abnormalities may contribute to the specific functional defects of the preparation.

Animals↗
PubMed1997

Effect of intratubular application of angiotensin 1-7 on nephron function.

Cleavage of the C-terminal tripeptide of angiotensin I (Ang I) by neutral endopeptidase 24.11 releases angiotensin 1-7 (Ang 1-7). Because Ang I and neutral endopeptidase 24.11 are present in proximal tubular fluid and brush border, respectively, Ang 1-7 could be released into proximal tubular fluid to affect nephron function. Therefore, we studied the effect of intratubular Ang 1-7 (10(-12) to 10(-8) M) on nephron function employing in vivo renal micropuncture in inactin-anesthetized Munich-Wistar-Frömter rats. We observed that: (i) Intratubular application of Ang 1-7 for 3, 15, or 30 min did not affect reabsorption in the microperfused proximal convoluted tubule determined as net fluid reabsorption. (ii) During perfusion of Henle's loop for 15 min with artificial tubular fluid (time control), we observed a decline in fluid, potassium and sodium reabsorption by 20, 18 and 5%, respectively. A similar decline in reabsorption was seen with intratubular application of Ang 1-7 in a concentration of 10(-12) or 10(-10) M. In contrast, intratubular application of Ang 1-7 in a concentration of 10(-8) M increased fluid, potassium and sodium reabsorption in that nephron segment by 11, 9 and 3%, respectively. The latter response was completely abolished by AT1 angiotensin II receptor antagonist losartan (10[-6] M). (iii) Intratubular application of Ang 1-7 did not affect net sodium, potassium, or fluid reabsorption in the distal tubule. (iv) TGF response assessed by measuring proximal tubular stop-flow pressure or single nephron filtration rate during orthograde open-loop perfusion of Henle's loop was not significantly altered by intratubular application of Ang 1-7. These findings show that intratubular application of Ang 1-7 in concentrations which possibly cover the physiological range does not significantly alter (i) tubular reabsorption in proximal convoluted or distal tubule, or (ii) TGF response. Intratubular Ang 1-7 at a concentration of 10(-8) M appears to increase reabsorption in Henle's loop by an AT1 angiotensin II receptor-mediated mechanism, the physiological relevance of which remains to be established.

Absorption↗
PubMed2004

Expression of somatostatin in the adult and developing mouse kidney.

BACKGROUND: Somatostatin (somatotropin release inhibiting factor) (SRIF) has potent antiproliferative and antisecretory actions. In the adult kidney, somatostatin alters renal blood flow, ion transport, and water permeability. While some evidence suggests that SRIF may be produced by adult kidney tubular cells, the specific tubules generating SRIF are unknown. Somatostatin has also been detected in a variety of embryonic tissues, although it has not been described in the developing kidney. Our objective was to determine the expression pattern of SRIF in both the adult and embryonic mouse kidney. METHODS: We performed reverse transcriptase-polymerase chain reaction (RT-PCR) and immunofluorescence for SRIF in developing and adult mouse kidney tissues. We localized SRIF by dual or serial labeling immunofluorescence with specific markers. RESULTS: Somatostatin mRNA was present in kidneys throughout embryogenesis and into adulthood. Starting at embryonic day (E) 12.5, SRIF was strongly expressed at the interface of the metanephric mesenchymal cells and the basolateral surfaces of ureteric bud trunks. Starting at E16.5, the staining at the interface was confined to the peripheral ureteric bud trunks and the clefts of newly dividing ureteric bud ampullae. In older embryos, SRIF also appeared in medullary tubules that appeared to be maturing thin descending limbs of Henle. In the adult kidney, SRIF proteins localized exclusively to medullary thin descending limbs of the Henle loop. CONCLUSION: In embryonic kidneys, SRIF is expressed first at the interface of the metanephric mesenchyme and basolateral ureteric bud and later in maturing thin descending limbs of Henle. Expression in the thin descending limb persists in the adult kidney.

Aging↗
PubMed1986

Further studies on oscillating tubulo-glomerular feedback responses in the rat kidney.

Free flow microperfusion (closed feedback loop) experiments in halothane-nitrous oxide-anaesthetized rats demonstrate two distinct oscillating TGF pressure responses to pertubations in early distal tubular flow. Flow rate changes of 2-8 nl min-1 induced a 0.02-0.03 Hz rhythm, while changes above 25 nl min-1 often induced a 0.17-0.18 Hz rhythm in proximal tubular pressures. Following interruption of microperfusion, the intratubular pressure showed an initial undershoot and a gradual oscillating return to the control level. Each nephron responded individually to systemic changes with oscillations differing in frequency, phase and amplitude from that of its neighbour. Postglomerular vascular pressure (PSV) oscillated synchronous with the proximal luminal pressure (PProx) of the same nephron; the amplitude of the PSV might be larger than that of the corresponding PProx. The PSV decreased by 2-3 mmHg as Henle loop flow was increased by 7 nl min-1. Furosemide (0.1-0.2 mM) in the microperfusate abolished the oscillations, and caused PSV and PProx to increase by 3-4 mmHg. This effect was rapidly reversible.

Animals↗
PubMed1986

Effects of various transport inhibitors on oscillating TGF pressure responses in the rat.

The present study examines the effect in free flow microperfusion experiments of various diuretics with different sites of action on an oscillating tubular pressure response to changes in Henle loop flow rate. Amiloride (1 mM) and bendroflumethiazide (0.1 mM) had no effect outside the stimulation caused by the solvent (Ringer solution). Acetazolamide (0.5 mM) stimulated a slow (30 mHz) oscillation and often activated a fast (130-190 mHz) rhythm. Furosemide (FUR) (0.1-2.0 mM) abolished the slow oscillation and caused the intratubular pressure to rise by 2-3 mm Hg. FUR (0.05 mM) caused partial inhibition of the slow rhythm, which usually became irregular. Bumetanide (BUM) (0.05 mM) elicited a biphasic response. Initially the pressure decreased, while the slow rhythm was amplified; then the fast oscillation was activated; after 4-6 min the oscillations disappeared, while the pressure increased. In the recovery period the oscillations often became irregular. The results confirm that the oscillating pressure response is mediated by a transport function of the macula densa (MD); and, thus, has the character of a tubulo-glomerular feedback (TGF) response. The data suggest 1. that BUM inhibition of NaCl co-transport in the cortical thick ascending limb of Henle (TAL) is delayed as compared to the medullary TAL; and 2. that FUR action at the MD interferes with more than one carrier mechanism. Partial inhibition gives rise to irregular oscillations.

Absorption↗
PubMed1987

Salidiuretic action of the calcium antagonist nitrendipine in dogs.

In an attempt to define the effects of a calcium antagonist, nitrendipine, on renal function, intrarenal hemodynamics, and renin release, we infused the drug into the renal artery of anesthetized dogs. Infusion of nitrendipine at a rate of 5 micrograms/min in both hydropenic and hydrated dogs resulted in a significant increase in renal blood flow (RBF), glomerular filtration rate (GFR), urine flow and renin release, with no change in systemic blood pressure, indicating a significant renal vasodilation. The urinary excretion rate of sodium increased by the same proportion as that of calcium. The intrarenal blood flow as measured by hydrogen washout rate showed that the outer cortical flow increased by the same proportion as the inner cortical flow. During nitrendipine infusion, free water reabsorption rate (TcH2O) in hydropenic dogs or free water clearance (CH2O) in hydrated dogs increased in proportion to the urine flow. Neither the ratio of TcH2O nor that of CH2O to osmolar clearance changed throughout the experiment. These data suggest that nitrendipine may not inhibit sodium transport in the medullary portion of the ascending limb of Henle and may induce an enhancement of the delivery of sodium to the Henle loop. Thus, nitrendipine exerts its diuretic and natriuretic actions via the alteration of renal hemodynamic and the inhibitory effect on proximal sodium reabsorption.

Animals↗
PubMed1990

Ultrastructural localization of IGF-I in the rat kidney; an immunocytochemical study.

We have shown recently by light microscopy that insulin-like growth factor I (IGF-I) immunoreactivity is localized in cells in the collecting ducts and in the thin loop of Henle in the normal rat kidney. In the present study, we have investigated the ultrastructural localisation of IGF-I using preembedding immunocytochemistry. The light microscopical findings were confirmed at the electronmicroscopical level. In collecting ducts as well as in the thin limb of Henle's loop a focal expression of IGF-I immunoreactivity was evident, i.e. distinctly IGF-I positive cells were intermingled with cells lacking IGF-I immunoreactivity. IGF-I immunoreactivity was found to have a diffuse cytoplasmatic distribution in both cell types. No specific association to organelles was found.

Animals↗
PubMed1987

Effect of volume depletion on the afferent arterioles in the avian kidney.

Nine white leghorn chickens were injected i.m. with furosemide (10 to 60 mg/kg body weight) twice daily for 18 days. The birds were then anesthetized with a combination of equithesin and diazepam and the kidneys perfused via the heart. Kidney tissue was sectioned serially and the granular epithelioid cells were counted in the juxtaglomerular apparatuses of the furosemide treated birds and in 3 normal chickens. Hyperplasia and hypergranulation of the epithelioid cells was found to occur in the juxtaglomerular apparatuses of both mammalian and reptilian type nephrons (with and without Henles loop) in the furosemide treated group. This finding was interpreted as an effect of hypovolaemia on the juxtaglomerular apparatuses. Furosemide caused an immediate stop in weight gain, an increase in the erythrocyte volume fraction and a sudden drop in blood pressure. The blood pressure later rose to subnormal levels. The heart rate was not altered. Plasma sodium and chloride fell significantly one day after furosemide administration and remained low throughout the experiment. Potassium fell during the second part of the experimental period. Captopril was injected after 18 days of furosemide treatment and lowered the blood pressure significantly. This was interpreted as indirect evidence for the presence of renin in the granular epithelioid cells and indicates the importance of the renin angiotensin system in maintaining the blood pressure in hypovolaemic conditions.

Animals↗
PubMed1984

Identification of a Na+,K+, Cl--cotransport protein of Mr 34 000 from kidney by photolabeling with [3H]bumethanide. The protein is associated with cytoskeleton components.

A polypeptide of Mr 34 000 is photolabeled with [3H]bumethanide after binding of this drug to membranes from the outer renal medulla and irradiation at 345 nm, a wavelength where bumethanide has an absorption maximum. Our data show that the polypeptide of Mr 34 000 is a component of the Na+/K+/Cl--cotransport system. The [3H]bumethanide binding protein is not extracted by concentrations of the nonionic detergent C12E8 that solubilizes 67% of the protein of the membranes including (Na+ + K+)-ATPase. This step increases the capacity for binding of [3H]bumethanide to 681 pmol/mg protein. Extraction of the binding protein requires high ionic strength suggesting that the Na+/K+/Cl--cotransport protein is associated with cytoskeleton components. This association may be important for control of the entry of NaCl into the cytoplasm and for cellular regulation of the rate of active transport of NaCl across the tubule cells in the thick ascending limb of Henles loop.

Animals↗
PubMed1985

Asymmetric orientation of amino groups in the alpha-subunit and the beta-subunit of (Na+ + K+)-ATPase in tight right-side-out vesicles of basolateral membranes from outer medulla.

The orientation of amino groups in the membrane in the alpha- and beta-subunits of (Na+ + K+)-ATPase was examined by labeling with Boldon-Hunter reagent, N-succinimidyl 3-(4-hydroxy,5-[125I]iodophenyl)propionate), in right-side-out vesicles or in open membrane fragments from the thick ascending limbs of the Henles loop of pig kidney. Sealed right-side-out vesicles of basolateral membranes were separated from open membrane fragments by centrifugation in a linear metrizamide density gradient. After labeling, (Na+ + K+)-ATPase was purified using a micro-scale version of the ATP-SDS procedure. Distribution of label was analyzed after SDS-gel electrophoresis of alpha-subunit, beta-subunit and proteolytic fragments of alpha-subunit. Both the alpha- and the beta-subunit of (Na+ + K+)-ATPase are uniformly labeled, but the distribution of labeled residues on the two membrane surfaces differs markedly. All the labeled residues in the beta-subunit are located on the extracellular surface. In the alpha-subunit, 65-80% of modified groups are localized to the cytoplasmic surface and 20-35% to the extracellular membrane surface. Proteolytic cleavage provides evidence for the random distribution of 125I-labeling within the alpha-subunit. The preservation of (Na+ + K+)-ATPase activity and the observation of distinct proteolytic cleavage patterns of the E1- and E2-forms of the alpha-subunit show that the native enzyme structure is unaffected by labeling with Bolton-Hunter reagent. Bolton-Hunter reagent was shown not to permeate into sheep erythrocytes under the conditions of the labeling experiment. The data therefore allow the conclusion that the mass distribution is asymmetric, with all the labeled amino groups in the beta-subunit being on the extracellular surface, while the alpha-subunit exposes 2.6-fold more amino groups on the cytoplasmic than on the extracellular surface.

Animals↗
PubMed1975

Role of prostaglandins in the pathogenesis of acute renal failure.

It is suggested that impaired glomerular infiltration in acute renal failure may be due, if only in part, to the derangement of a normal local feedback mechanism involving prostaglandins. According to this hypothesis, prostaglandins made in the medulla normally enter the loop of Henle and thus are present in distal tubule fluid reaching the macula densa. In the absence of direct vascular channels connecting the renal medulla with the outer cortex, this may be the only route by which medullary prostaglandins can reach the cortex without being destroyed by dehydrogenases. Under most circumstances in which renal perfusion and glomerular filtration fall, flow through Henle's loop continues, albeit at a reduced rate. This slowed flow through the loop and augmented prostaglandin release combine to produce a high concentration of prostaglandin in fluid leaving the medulla which, acting on the macula densa, counteracts the vasoconstrictor stimulus. If, however, filtration stops completely because of overwhelming vasoconstriction, flow along the loop also stops ans prostaglandins no longer reach the macula densa. Thus, the prostaglandin feedback loop would be opened, constrictor mechanism remain unchecked, and filtration failure perpetuated. It is proposed that such a self-perpetuating mechanism might operate in acute renal failure.

Acute Kidney Injury↗
PubMed2006

[Polyuria].

Beyond polyuria following psychogenic polydipsia, in a more narrow sense, this condition may be classified into impaired water re-absorption (i) due to tubular injury or (ii) relative or absolute loss of function of antidiuretic hormone (ADH). Tubular injury may be caused by different toxins affecting the ascending Henle loop as hypercalciuria, drugs and antibiotics as tubular necrosis. ADH deficiency, either absolute or relative, occurs with central or peripheral diabetes insipidus, which is based on synthesis failure or loss of peripheral efficacy of ADH due to receptor malfunction. Diagnosis of polyuria rests upon a thirst challenge in conjunction with laboratory studies of osmolality in serum and urine, which discloses the non-function of the hypothalamic-renal axis. Administration of ADH may differentiate between central and peripheral diabetes insipidus.

Humans↗
PubMed1996

High resolution localization of endothelin receptors in rat renal medulla.

The cellular localization of endothelin receptors in the inner medulla of the rat kidney was investigated by using high resolution light and electron microscopic autoradiography, with the microwave irradiation fixation methods. Kidney slices were incubated with 125I-endothelin-1 alone or with selective ligands for the endothelin ETB and/or ETA receptors for light microscopic autoradiography. At the microscopic level, 125I-endothelin-1 was found to bind specifically to the glomeruli, arterioles and peritubular spaces in the cortex and vasa recta and surrounding tissues in the inner medulla. These bindings were also observed when the tissue slices were incubated in the presence of IRL1620 (ETB receptor agonist) or 97-139 (ETA receptor antagonist). Electron microscopic autoradiography using 125I-endothelin-1 in the inner medulla revealed silver grains over endothelial cells of the vasa recta and interstitial and collecting duct cells. No grains were detected over inner lining cells of the thin limbs of Henle's loop. These interstitial cells contained abundant microorganelles and lipid droplets, and had extensive cytoplasmic processes that closely related to the basement membranes of the vasa recta and loop of Henle. These findings demonstrate that type 1 interstitial cells are also primary sites for endothelin receptors as well as endothelial cells of the vasa recta and collecting duct cells in the inner medulla.

Animals↗