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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium transport across luminal membranes of proximal tubules isolated from the kidney cortex of young, prehypertensive rats of the Milan hypertensive strain (MHS) and their corresponding normotensive controls, the Milan normotensive strain (MNS), was measured. A higher sodium uptake was observed in vesicles from MHS, although membrane preparations from both strains behaved similarly as far as enzyme profile and sodium-dependent glucose transport were concerned. In the presence of an inwardly directed sodium gradient, sodium uptake depended on the relative permeability of the counterion: in the presence of 100 mM NaCl, sodium transport in MHS was 26% higher than that in normotensive controls (p less than 0.05). Also, a significantly faster sodium uptake by membrane vesicles from MHS was observed when a pH gradient and an electrical potential difference (inside-negative) were imposed across the membrane. In this condition, sodium uptake by membrane vesicles from MHS was up to 39% higher than that in control MNS (p less than 0.01). Therefore, the difference in sodium transport observed between preparations of luminal membrane from the proximal tubule of MNS and MHS seems to be due to a higher rheogenic sodium pathway in the MHS. The present results are in keeping with previous data showing an increased sodium transport across renal tubules of the MHS and support the hypothesis that the abnormality in sodium and water handling by kidneys from MHS can be related to an alteration in sodium transport across the luminal membrane of the proximal tubule cells.
Hypertension 1986 Oct
PMID:Sodium and glucose transport across renal brush border membranes of Milan hypertensive rats. 375 27

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3-6.9 mmol/l), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mmol/l), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/h), high plasma aldosterone level (32-100 ng/dl), and normal glomerular filtration rate (131 ml/min/1.73 m2). During the hyperkalemic period, urine was highly acidic (pH 4.6-5.0), urinary NH4 excretion (10-13 microEq/min) and urinary net acid excretion (19-24 microEq/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, the maximal tubular HCO3 reabsorption was markedly diminished (19.8 mmol/l glomerular filtrate), and the fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized was 20%. Urine minus blood PCO2 increased normally during NaHCO3 infusion (31 mm Hg), and the urinary pH remained maximally low (less than 5.3) when the buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while the urinary pH remained maximally low (4.9-5.2), the maximal tubular HCO3 reabsorption returned to normal values (24.8 mmol/l glomerular filtrate), and FE HCO3 at normal plasma HCO3 was 1%. Nasal insufflation of 1-desamino-8-D-Arginine Vasopressin (dDAVP) resulted in an acute normalization of the renal handling of K and in an increase in net urinary acid excretion. We conclude that: the effect of dDAVP on renal handling of K may be explained by the reversal of the distal chloride shunt and/or an increase in luminal membrane conductance to K; the distal acidification seems to be normal which in the event of distal chloride shunt impairing distal hydrogen secretion might be explained by the presence of systemic acidosis which is a potent stimulus of hydrogen secretion, and metabolic acidosis in the steady state was accounted for by the diminution of bicarbonate reabsorption and ammonia production in the proximal tubule secondary to chronic hyperkalemia.
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PMID:Pseudohypoaldosteronism type II: proximal renal tubular acidosis and dDAVP-sensitive renal hyperkalemia. 377 34

The function of the short loops of Henle was investigated by micropuncture technique in normal rats, in rats with spontaneous hypertension, and in the untouched kidney of rats with experimental renal hypertension. All animals received a standard infusion of 1.2 ml of isotonic saline per hr. With increasing arterial blood pressure (range from 90 to 220 mm Hg), a continuous decrease in transit time of Lissamine green through Henle's loop from 32 to 10 sec was observed. Fractional water reabsorption along the loop declined progressively from 26 to 10%, and fractional sodium reabsorption decreased from 40 to 36% of the filtered load. The fluid volume in Henle's loop calculated from transit time and mean flow rate also decreased with increasing blood pressure. There was no change in superficial single nephron filtration rate but there was a slight increase in total glomerular filtration rate (GFR). Sodium and water reabsorption in the proximal tubule remained unchanged. Urine flow rate, sodium excretion, osmolar clearance, and negative free water clearance increased with increasing blood pressure. The osmolal urine to plasma (U/P) ratio declined but did not fall below a value of 1.5. It is concluded that the increase in sodium and water excretion with chronic elevation of arterial blood pressure is caused by a decrease of sodium and water reabsorption along the loop of Henle, presumably as a consequence of increased medullary blood pressure.
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PMID:Fluid reabsorption in Henle's loop and urinary excretion of sodium and water in normal rats and rats with chronic hypertension. 542 22

The effect of acute hypertension on sodium reabsorption by the proximal tubule was studied in rats by means of micropuncture methods. Hypertension was induced by bilateral carotid artery ligation and cervical vagotomy. Within a few minutes after blood pressure rose (30-60 mm Hg above control levels), a moderate natriuresis and diuresis began. Proximal sodium reabsorption, measured by two independent methods, was found to be markedly suppressed, both in absolute amount per unit length and per unit of tubular volume (C/pir(2)). The ratio between tubular volume and glomerular filtration rate (GFR) (pir(2)d/V(0)) was found to be increased. These observations indicate that the inhibition of proximal sodium reabsorption induced by hypertension cannot be explained by the tubular geometry hypothesis of sodium regulation. Several possible hormonal mechanisms were investigated. Intravenous d-aldosterone did not prevent the suppression of sodium transport due to acute hypertension, nor did chronic oral saline loading to reduce the renal content of renin. Constriction of the suprarenal aorta, with maintenance of a normal renal perfusion pressure, did prevent the inhibition of proximal transport during carotid artery occlusion, thus excluding an extrarenally produced natriuretic hormone as the mechanism. The observations are compatible with the view that sodium transport was inhibited either by an intrarenal natriuretic hormone or by an increase in the interstitial volume of the kidney produced by a transient hydrostatic pressure gradient across the peritubular capillaries. The latter seems more likely to us because of the rapidity of onset of the natriuresis, and because removing the renal capsule and releasing the surface interstitial fluid prevented the effect of hypertension on proximal sodium transport.
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PMID:Effect of acute hypertension on sodium reabsorption by the proximal tubule. 565 96

To evaluate the effects of saline loading on distal sodium reabsorption in hypertensive man, studies were performed during both water deprivation and water diuresis in eight hypertensive subjects, and the results were compared to data obtained from similar studies in normal subjects. All hypertensive patients exhibited an enhanced excretion of filtered sodium (C(Na)/C(In)) at any level of distal delivery of sodium compared to normal controls. Free water reabsorption (T(c) (H2O)) during hypertonic saline loading was quantitatively abnormal in the hypertensives at high levels of osmolar clearance (C(Osm)), and also the curve of T(c) (H2O) vs. C(Osm) leveled off above a C(Osm) of 18 ml/min per 1.73 m(2) in the hypertensive group in contrast to the normal controls in whom T(c) (H2O) showed no evidence of achieving an upper limit. Sodium depletion exaggerated the abnormality in T(c) (H2O) in hypertensives, and resulted in a positive free water clearance (C(H2O)) during hydropenia. During hypotonic saline loading in water diuresis, changes in free water clearance per 100 ml of glomerular filtrate (C(H2O)/C(In)) were less at any given increment in urine flow per 100 ml of glomerular filtrate (V/C(In)) in the hypertensives compared to normal controls (P < 0.001). This abnormality in C(H2O)/C(In) in the hypertensives in conjunction with the defect in T(c) (H2O) observed during hydropenia indicates that sodium reabsorption in the loop of Henle was abnormal at any given rate of distal delivery of sodium in hypertension. Furthermore, these abnormalities in T(c) (H2O) and C(H2O) coincided temporally with the development of the exaggerated natriuresis. Although the distal defect in sodium transport, in large part, accounted for the augmented natriuresis in hypertension, evidence was present also for enhanced rejection of sodium in the proximal tubule during saline loading in the hypertensives. Additional studies utilizing acetazolamide which increases distal delivery of sodium without extracellular fluid volume expansion showed only minimal abnormalities in C(H2O) in the hypertensive group, indicating that the defect in sodium transport in the loop of Henle in hypertensives is mainly an abnormal response to extracellular fluid expansion rather than an intrinsic defect in the loop to handle increased tubular loads of sodium. It is possible that the abnormality in sodium reabsorption in the loop of Henle is due to the transmission of the abnormally elevated blood pressure of the hypertensives to the medullary vasa recta during saline loading.
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PMID:Mechanism of exaggerated natriuresis in hypertensive man: impaired sodium transport in the loop of Henle. 577 Nov 85

In contrast to healthy persons, microvillous antigens of the proximal tubule were excreted at an increased rate in patients with kidney diseases as could be shown using specific antisera against brush border (BB) fragments (tissue-proteinuria, histuria). These urinary membrane components were immunologically completely identical with those antigens prepared from isolated kidney cell membranes. A glycoprotein of 240 000 dalton, containing mannose and N-acetylglucosamine was identified as a major immunoreactive constituent of the brush border surface and found to be part of a multienzyme complex. BB-antigens were excreted in urine of patients with glomerulonephritis, hypertension, pyelonephritis, multiple myeloma, after operations, after kidney transplantation, under cytostatic treatment, and after administration of radiopaque agents. Histuria of BB-antigens was significantly higher in patients with multiple myeloma and Bence-Jones-proteinuria compared to those patients where no Bence-Jones L-chains in urine became apparent. Selective kidney angiography and intravenous urography caused a significantly higher output of BB-antigens as compared to the control period (2 p less than 0,005). In a volunteer model, on the basis of BB-histuria, a different nephrotoxic potency of cephalosporins and aminoglycosides arose. In addition, beside soluble BB-antigens, also high molecular weight membrane vesicles were discovered in urine of patients after cytostatic treatment (cis-platinum), after x-ray contrast media, and after kidney transplantation. Both, soluble as well as supramolecular membrane vesicles were isolated from urine applying immunospecific affinity chromatography (anti-BS-agarose beads). Labeled antisera directed against the vesicle material of urine revealed a specific immunofluorescence of cortical tubule only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunodiagnosis of kidney tubular cell injuries using specific anti-membrane antibodies]. 638 21

Diuretics have a central role in the treatment of edema and hypertension. This function is primarily an induction of a net negative balance of solute and water. Reviewed herein are the transport properties of each nephron segment that governs salt and water reabsorption with specific reference to the mechanisms by which the various diuretic agents affect those transport processes. Under normal circumstances, the proximal tubule reabsorbs about 50 to 66 percent of the filtered fluid by both active and passive mechanisms. However, diuretics that inhibit proximal reabsorption are "weak" diuretics since distal compensatory mechanisms can overcome their effect. The thin descending limb of Henle is highly permeable to water and relatively impermeable to solutes. Thus, its main physiologic function is to allow osmotic water abstraction. Although diuretics have no direct epithelial effect on this segment, many of the diuretics decrease fluid reabsorption from it by abolishing the papillary osmotic gradient. The decreased water absorption from the descending limb of Henle has a major role in over-all increased diuresis since nephron segments distal to the descending limb are impermeable to water in the absence of vasopressin. The thin ascending limb of Henle is impermeable to water while being highly permeable to sodium and chloride. Diuretics have no direct effect on the thin ascending limb of Henle. The medullary and cortical segments of the thick ascending limb of Henle absorb sodium chloride by active mechanisms as a result of a secondary active chloride transport mechanism that depends on the presence of sodium (co-transport mechanism). This transport mechanism is located on the luminal membrane. Most of the "loop" diuretics effect this process from the luminal side by having a direct inhibitory effect on this co-transport process. The diuretics that have a primary effect on the medullary segment (furosemide, bumetanide, ethacrynic acid) inhibit the concentrating mechanisms, whereas the diuretics that are effective primarily in the cortical segment (thiazides plus the diuretics affecting the medullary segment) inhibit the urinary diluting mechanism. The loop diuretics are physiologically the most potent family of diuretics. The cortical collecting duct segment reabsorbs sodium by active mechanisms. These processes are stimulated by aldosterone. The diuretics that affect these processes are considered weak diuretics, but they do have the metabolic effect of potassium sparing.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Site and mechanism of action of diuretics. 649 55

The results of a study carried out on 32 patients with arterial hypertension about nephrotoxic effect obtained with a new non-ionic contrast agent have been reported. The diagnostic approach was based on the determination of the urinary excretion of two characteristic enzymes of the proximal tubule-epithelial cells (alfa-glycosidase and gamma-glutamil-transferase) and of a microprotein (beta-2-microglobulin) filtered by glomeruli and readsorbed and catalized by epithelial cells. The method used show an increased sensitivity and reliability in the early recognition of a kidney damage as well as in the control of anatomic and functional changes, in comparison with the classic parameters (azotemia, creatininemia). The results show a significantly lower enzymuric and microproteinuric level using non-ionic contrast media, also, in the patients at relatively higher risk of kidney damage. This results should be interpreted in favour to a lower potential nephrotoxicity of non-ionic contrast media and their elective use in the patients with a higher risk of kidney damage.
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PMID:[Renal contrast radiography study in hypertensive patients: comparison of the nephrotoxicity of ionic and non-ionic contrast media]. 666 40

Fractional excretion of lithium, as a marker for proximal sodium reabsorption, was determined in normotensive Dahl S rats (susceptible to NaCl hypertension) and Dahl R rats (resistant to NaCl hypertension) before and following an acute sodium load. Baseline mean arterial pressures, inulin clearances, sodium excretion rates, and fractional lithium clearances were not different between the R and S rats. Following the salt loading and despite similar mean arterial pressures and degree of volume expansion, the glomerular filtration rate, urinary flow rates, and absolute sodium excretion rates were greater in R than S rats. The fractional excretion of lithium was also greater in R than S rats. These data demonstrate that, at equal mean arterial pressures, Dahl S rats have a reduced capacity for sodium excretion, and that this defect is present prior to the development of hypertension. Furthermore, the observation that these animals also have a lower fractional lithium excretion during volume expansion suggests that salt loading reduces proximal tubule reabsorption to a lesser extent in Dahl S than R rats. These data suggest that the subnormal sodium and water excretion observed after sodium loading in S rats may be partially due to an abnormality in proximal tubule sodium handling.
Hypertension
PMID:Differential effect of salt loading on sodium and lithium excretion in Dahl salt-resistant and -sensitive rats. 673 61

Physical factors, and renal interstitial hydrostatic pressure in particular, have an important effect on sodium excretion by the kidney. Changes in hydrostatic and oncotic pressures in the peritubular microcirculation may have effects on proximal tubule reabsorption under some, but not all, circumstances. In regard to control of sodium excretion, the loop of Henle may be a particularly important segment which is sensitive to transepithelial hydrostatic pressure changes. There is little evidence to support an effect of physical factors on sodium reabsorption by the distal tubule. The collecting tubule may be another pressure-sensitive site; however, changes in sodium reabsorption by deep nephrons in the kidney may account for changes that have been attributed to the collecting duct. Changes in intrarenal pressure may be an important link in the regulation of sodium excretion, particularly in pathological circumstances, such as the exaggerated natriuresis of hypertension and the sodium retention seen in congestive heart failure.
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PMID:Role of hydrostatic and oncotic pressures in renal sodium reabsorption. 685 Oct 4


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