Study of Chloride Transport Across the Rabbit Cortical Collecting Tubule

Recent micropuncture studies have suggested that the collecting tubule may be involved in the regulation of extracellular fluid volume. The present studies were designed to evaluate chloride transport across the in vitro-perfused rabbit cortical collecting tubule inasmuch as chloride ion would ultimately affect extracellular fluid volume. The tubules were perfused and bathed with artificial solutions simulating ultrafiltrate. Four groups of studies were conducted. In groups one and two, tubules from rabbits not receiving desoxycorticosterone (DOCA) were compared to tubules from rabbits which had received DOCA (5 mg/day) for 1 wk. In groups three and four, tubules were obtained only from rabbits not receiving DOCA. In group one, sequential bidirectional chloride fluxes were measured. The ratio of chloride efflux to influx was 0.99±0.04 in tubules obtained from rabbits not receiving DOCA whereas it was 1.28±0.09 in tubules obtained from rabbits receiving DOCA, suggesting stimulation of net chloride flux under these conditions. In group 2, chemical chloride concentration and osmolality of the collected fluid were measured. Neither the chemical chloride concentration nor the osmolality of the collected fluid decreased significantly below their respective perfusion fluid values in tubules from non-DOCA-treated rabbits but there was a significant decrease in the chemical chloride concentration (10-42 meq/liter) and osmolality (10-42 mosmol/kg H₂O of the collected fluid in tubules from DOCA-treated rabbits. In group three, unidirectional chloride permeabilities from lumen-to-bath were determined during the passage of current down the perfusion pipette. The alterations of the average lumen potential, −35±4 and +28±2 mV, did not influence unidirectional chloride movement suggesting that the cortical collecting tubule is quite impermeable to chloride. In group four, unidirectional chloride permeability from lumen-to-bath was measured before and after substitution of NaCH₃SO₄ for sodium chloride in the bath. Replacement of chloride by CH₃SO₄ reversibly decreased the apparent chloride permeability from 2.41±0.50 to 0.69±0.08 (×10⁻⁵ cm/s) demonstrating that ³⁶Cl permeability is dependent on the chemical concentration of chloride.     

Hypoxanthine Uptake in Isolated Rat Renal Cortical Tubule Fragments

Isolated renal tubule fragments prepared from adult Sprague-Dawley rats were used to study the cellular uptake of hypoxanthine. This uptake was rapid, reaching a steady state after 30 min of incubation. Analysis of the intracellular pool during the initial uptake and at the steady state revealed a concentration gradient of hypoxanthine consistent with active transport, although only one-third of the transported hypoxanthine remained unmetabolized. The remainder of the transported hypoxanthine was converted to inosine and inosinic acid, but detectable conversion to uric acid was not noted. A kinetic analysis of uptake revealed that two systems for cellular entry of hypoxanthine existed with K(m1) = 0.005 and K(m2) = 0.80 mM. Hypoxanthine uptake at physiologic concentrations was oxygen, sodium, and temperature dependent, but the addition of metabolic fuels and alteration of the medium pH over the range of from 6.1 to 7.4 had no effect. Adenine, guanine, and inosine inhibited the uptake of hypoxanthine via the low-K(m) system which mediates the majority of uptake at physiologic levels. Xanthine, uric acid, and probenecid inhibited uptake via the high-K(m) system, but did not affect uptake via the low-K(m) system. The data indicate that hypoxanthine at physiologic levels is transported into the renal tubule cell via a system different from that for other oxypurines.     

Characteristics of the Relationship between the Flow Rate of Tubular Fluid and Potassium Transport in the Distal Tubule of the Rat

The flow rate of tubular fluid has been suggested as one of several factors which may influence potassium transport in the distal convoluted tubule of the kidney. In the present micropuncture studies, the relationship between the flow rate of distal tubular fluid and potassium transport was examined in four groups of rats. Three groups of rats (I, II, and IV) were fed normal rat chow before study whereas one group (III) was fed chow containing 10% KCl. Group II received 10-20 mug/kg per h of d-aldosterone throughout the study. Distal tubular potassium transport in groups I, II, and III was examined before and after an increase in the flow rate of distal tubular fluid as induced by the infusion of an isotonic saline-bicarbonate solution equivalent to 10% of body weight. In group IV, distal tubular potassium transport was examined before and after enhancement of the flow rate by the infusion of hypertonic (15%) mannitol.In all four groups, distal tubular potassium secretion increased as the flow rate of tubular fluid increased. The nature of the relationship between distal tubular potassium transport and tubular fluid flow rate, however, was influenced by the extent to which the tubular fluid to plasma potassium ratio in the late distal tubule varied as the flow rate increased. As the flow rate was increased this ratio decreased significantly and to a comparable extent in groups I and II. In groups III and IV, on the other hand, this ratio was essentially identical during hydropenia and after the increase in the flow rate of tubular fluid. As a result, the increment in the amount of potassium present at the late distal tubule, which occurred as the flow rate increased, was significantly greater in groups III and IV than in groups I and II. The contrast in the relationship between the flow rate of distal tubular fluid and potassium transport which were observed, probably reflects differences in the net driving force for cell to lumen potassium movement. Seemingly, the net driving force for potassium movement was maintained, as the flow rate of tubular fluid increased, by chronic potassium loading in group III and by hypertonic mannitol infusion in group IV. In groups I and II, the net driving force for potassium movement decreased as the flow rate of tubular fluid increased. However, the net driving force did not decrease in proportion to the increase in flow rate since potassium secretion was increased by increments in flow rate in these groups as well.We conclude that our results are consistent with the view that the flow rate of tubular fluid is a factor which can affect distal tubular potassium transport. However, the nature of the relationship between the flow rate of tubular fluid and potassium transport appears to depend upon the degree to which the driving force for cell to lumen potassium movement changes as the flow rate is varied.     

Effects of Ethacrynic Acid on the Isolated Collecting Tubule

Effects of the diuretic ethacrynic acid on osmotic water permeability were investigated in the isolated perfused collecting tubule of the rabbit kidney.The base-line water permeability of the collecting tubule was not affected when the drug (10(-4)M) alone was added to the bathing medium. Vasopressin alone in the bathing medium (2, 5 muU/ml) elicited a significant increase in osmotic water absorption. With vasopressin kept in the bathing medium, the addition of 10(-5)M ethacrynic acid depressed the hydro-osmotic effect of vasopressin by 50%. This inhibitory effect of low concentrations of ethacrynic acid could be surmounted by high, supramaximal dosage levels of vasopressin.When 10(-4)M ethacrynic acid was added to the bathing medium before vasopressin, the hydro-osmotic effect of vasopressin and the diuretic in combination was insignificant.Dibutyryl adenosine 3'5'-monophosphate (10(-4)-10(-2)M) alone in the bathing medium significantly increased baseline osmotic water flow, mimicing the effect of antidiuretic hormone. When ethacrynic acid was added together with the nucleotide, the permeability remained at the same high level. Theophylline, like the nucleotide and vasopressin, produced a significant hydro-osmotic effect. The magnitude of this response was not affected by further addition of ethacrynic acid (10(-4)M).It was concluded that ethacrynic acid is an antagonist of antidiuretic hormone. The antagonism probably occurs at the level of the receptor site of the hormone on the peritubular membrane. Antagonism to circulating antidiuretic hormone may therefore be one of the factors involved in the loss of renal concentrating ability brought about by ethacrynic acid diuresis.     

Effects of Acute Bilateral Ureteral Obstruction on Deep Nephron and Terminal Collecting Duct Function in the Young Rat

The effects of acute bilateral ureteral obstruction (BUO) of 18-h duration on deep nephron and collecting duct function were studied by micropuncture in 11 weanling rats. After release of BUO glomerular filtration rate was reduced (178±15 vs. 1,343±119 μl/min per g kidney weight in shams), while urine flow was increased averaging 17.5±1.3 vs. 6.8±0.72 μl/min per g kidney weight in controls. There was a marked increase in the absolute and fractional excretion of Na. Single nephron glomerular filtration rate of deep nephrons was reduced in the BUO group, mean 19.4±3.5 vs. 77.0±7.7 nl/min per g kidney weight in shams. Single nephron glomerular filtration rate of superficial nephrons fell to the same extent after relief of BUO. Mean tubular fluid to plasma inulin ratio of fluid from Henle's loop was 2.46±0.20 after relief of BUO vs. 8.23±0.85 in shams. This suggested a reduction in the reabsorption of Na and water before the bend of the loop of Henle, most likely in both the proximal tubule and descending limb. Fluid osmolality was depressed due to a decline in both Na and nonelectrolyte solute content. After release of BUO the percentage of filtered water remaining in the collecting duct (CD) at the base of the papilla was greater than in controls (13.3±2.0 and 1.72±0.01%, respectively) but fell significantly by the tip of the papilla to 7.92±1.12 vs. 1.17±0.02% in controls. These results indicate that water was reabsorbed along the terminal CD after relief of ureteral obstruction. In fact, a greater fraction was reabsorbed in this segment after release of BUO (5.37±1.58%) than after sham operation (0.55±0.15%). Similar changes were seen in Na excretion. Thus alterations in deep nephron function appear to contribute to the natriuresis and diuresis which follow release of BUO while terminal CD function in this model appears intact.     

Collecting Duct Sodium Reabsorption in Deoxycorticosterone-Treated Rats

In vitro studies of isolated, perfused, cortical collecting tubules have demonstrated that prior chronic deoxycorticosterone acetate (DOCA) treatment increases sodium reabsorption in this nephron segment, yet sodium balance in vivo is maintained. To evaluate the effect of chronic DOCA treatment on collecting duct sodium reabsorption in vivo, we compared fractional sodium delivery (FD(Na)%) out of the superficial late distal tubule with the fraction of sodium remaining at the base and the tip of the papillary collecting duct during extracellular fluid volume expansion in untreated, salt-treated, and DOCA-salt-treated rats. In untreated rats, FD(Na)% to the distal tubule was 6.5+/-1.0%, and to the base was 8.7+/-1.6% (Delta2.2+/-0.9%, P < 0.05). FD(Na)% to the tip was 4.9+/-1.1%, significantly less than FD(Na)% to the base (Delta3.7+/-1.1%, P < 0.01). In salt-treated rats, FD(Na)% to the distal tubule was 8.3+/-0.8%, and to the base was 10.4+/-1.1%. FD(Na)% to the tip was 5.9+/-0.6%, significantly less than FD(Na)% to the base (Delta 4.6+/-1.0%, P < 0.005). In DOCA-salt-treated rats, FD(Na)% to the distal tubule was 16.1+/-2.6% and to the base was 9.5+/-1.9% (Delta 6.6+/-1.7%, P < 0.005). FD(Na)% to the tip was 5.9+/-1.2%, also significantly less than FD(Na)% to the base (Delta 3.6+/-1.1%, P < 0.01). We conclude that (a) in DOCA-salt-treated rats, sodium delivery to the end of the superficial distal tubule is greater than in untreated or salt-treated rats; (b) in DOCA-salt-treated rats, sodium delivery to the end of the superficial distal tubule is greater than to the base of the papillary collecting duct, suggesting stimulation of sodium reabsorption in the cortical and(or) outer medullary collecting duct; and (c) sodium reabsorption by the papillary collecting duct is unaffected by chronic DOCA-salt treatment in the volume-expanded rat.     

Bicarbonate Secretion by Rabbit Cortical Collecting Tubules in Vitro

We previously reported that rabbit renal cortical collecting tubules can secrete bicarbonate in vitro (i.e., there can be net transport from bath to lumen, causing the concentration in the lumen to increase). Net bicarbonate secretion was observed most often when rabbits had been pretreated with NaHCO₃ and were excreting alkaline urine before being killed for experiments. The purpose of the present studies was to elucidate the mechanism involved by testing the effects of ion substitutions and drugs on collecting tubules that were secreting bicarbonate. Acetazolamide inhibited net bicarbonate secretion, suggesting that the process is dependent upon carbonic anhydrase. Net bicarbonate secretion also decreased when sodium in the perfusate and bath was replaced by choline, but not when chloride was replaced by nitrate or methylsulfate. Ouabain had no significant effect. Amiloride caused net bicarbonate secretion to increase. The rate of net secretion did not correlate with transepithelial voltage. The results are compared to those in turtle urinary bladders that also secrete bicarbonate. There are no direct contradictions between the results in the two tissues, i.e., in turtle bladders acetazolamide also inhibited bicarbonate secretion and ouabain had no effect. Nevertheless, it seems unlikely that net secretion of bicarbonate by collecting tubules involves specific exchange for chloride, as has been proposed for turtle bladders, because replacement of chloride by other anions did not inhibit bicarbonate secretion by collecting tubules. It was previously shown that the collecting tubules in vitro also may absorb bicarbonate, especially when the rabbits have been treated with NH₄Cl and are excreting acid urine before being killed. The effects of drugs on net bicarbonate secretion found in the present studies are compared to their previously reported effects on net bicarbonate absorption and the possibility is discussed that bicarbonate absorption and secretion are independent processes, as was previously proposed for turtle bladders.     

A Microperfusion Study of Bicarbonate Accumulation in the Proximal Tubule of the Rat Kidney

In order to determine whether HCO₃^- gains access to the proximal tubular lumen from a source other than the glomerular filtrate, we carried out microperfusion experiments on isolated segments of rat proximal tubules in vivo. The perfusion fluid was essentially free of HCO₃^- and of a composition that prevented net absorption of sodium and water.     

Vascular Effects of Arginine Vasopressin during Fluid Deprivation in the Rat

The vascular effects of arginine vasopressin (AVP) were examined in conscious Sprague-Dawley rats. In six control rats, synthetic AVP at a dose of 40 ng/kg, injected as an intravenous bolus, resulted in a rise in mean arterial blood pressure (BP) from 127 to 149 mm Hg (P < 0.005). No tachyphylaxis was observed after a second AVP bolus administered 30 min later, as BP increased from 125 to 150 mm Hg, P < 0.005. In a second group of six rats, 1-deamino penicillamine, 2-(O-methyl) tyrosine AVP ([dPTyr (Me)]AVP), was administered intravenously at a dose of 10 μg/kg, just before the second AVP bolus. In this group of studies BP rose from 124 to 150 mm Hg (P < 0.01) after the first AVP bolus, but not after the second AVP bolus, which was administered after [dPTyr (Me)]AVP (129 vs. 129 mm Hg, NS). To assess the effect of this AVP pressor antagonist on BP in rats with suppressed endogenous vasopressin, six water-diuresing rats (mean urinary osmolality, 99 mosmol/kg H₂O) were administered the analogue at the same dose as the first group of rats. The analogue exerted no demonstrable effect on mean BP (128 before vs. 129 mm Hg after [dPTyr (Me)]AVP, NS). In these rats, mean radioimmunoassayable levels of AVP were at or below the detectable limits of our assay (0.5 pg/ml). In contrast, six rats in which endogenous AVP was stimulated by fluid deprivation for 24 h (mean urinary osmolality, 2,489 mosmol/kg H₂O and mean AVP level of 21.6 pg/ml) had a marked fall in BP when administered the AVP analogue. In these animals [dPTyr (Me)]AVP caused a fall in BP from 124 to 110 mm Hg (P < 0.005). This fall in blood pressure was due to a fall in peripheral vascular resistance (0.35 vs. 0.30 mm Hg/ml per min per kg, P < 0.02) after [dPTyr (Me)]AVP, as cardiac index remained unchanged.     

Effects of Anion-Transport Inhibitors on NaCl Reabsorption in the Rat Superficial Proximal Convoluted Tubule

The effects of anion-transport inhibitors on volume reabsorption, and total CO(2) concentrations were examined by in vivo microperfusion of superficial proximal convoluted tubules of rats. The luminal perfusion solution was a high-chloride, low-bicarbonate solution like that in the in vivo late proximal tubule. The anion-transport inhibitors were only added to the luminal perfusion solutions.In tubules perfused with the control high-chloride solution, the rate of volume reabsorption (J(v)) was 2.3+/-0.2 nl/mm.min (n = 18), and the collected total CO(2) concentration was 4.0+/-0.3 mM. Furosemide (3 mM) caused a marked reduction in volume reabsorption to 0.8+/-0.3 nl/mm.min (n = 20) and only a slight increase in the total CO(2) concentration of collected samples of perfusate (7.8+/-0.5 mM). 0.8 mM acetazolamide caused a more pronounced rise in the collected total CO(2) concentrations to 10.7+/-0.5 mM but only a slight fall in J(v) to 1.7+/-0.3 nl/mm.min (n = 19). Hence, we inferred that inhibition of carbonic anhydrase only partially accounted for the inhibition of J(v) by furosemide. 4-acetamido-4'-iso-thiocyanato-stilbene-2,2'-disulphonic acid (0.1 mM), a well-characterized inhibitor of erythrocyte anion exchange mechanisms, also reduced J(v) to 1.6+/-0.3 nl/mm.min (n = 15) without changing the total CO(2) concentrations of the collected perfusates (3.6+/-0.4 mM). The effect of 4-acetamido-4'-iso-thiocyanato-stilbene-2,2'-disulphonic acid on volume reabsorption could not be explained by carbonic anhydrase inhibition because there was no increase in the total CO(2) concentration of the collected fluids. Furosemide did not significantly inhibit the rate of tracer glucose efflux out of the tubules, which suggests that the effect of furosemide on volume reabsorption was not a result of some nonspecific depression of active sodium transport. These results are discussed with respect to the possible effects of anion-transport inhibitors on the paracellular shunt pathway, active sodium reabsorption, and neutral sodium chloride transport.     

Temporomandibular Disorder Modifies Cortical Response to Tactile Stimulation

Individuals with temporomandibular disorder (TMD) suffer from persistent facial pain and exhibit abnormal sensitivity to tactile stimulation. To better understand the pathophysiological mechanisms underlying TMD, we investigated cortical correlates of this abnormal sensitivity to touch. Using functional magnetic resonance imaging (fMRI), we recorded cortical responses evoked by low-frequency vibration of the index finger in subjects with TMD and in healthy controls (HC). Distinct subregions of contralateral primary somatosensory cortex (SI), secondary somatosensory cortex (SII), and insular cortex responded maximally for each group. Although the stimulus was inaudible, primary auditory cortex was activated in TMDs. TMDs also showed greater activation bilaterally in anterior cingulate cortex and contralaterally in the amygdala. Differences between TMDs and HCs in responses evoked by innocuous vibrotactile stimulation within SI, SII, and the insula paralleled previously reported differences in responses evoked by noxious and innocuous stimulation, respectively, in healthy individuals. This unexpected result may reflect a disruption of the normal balance between central resources dedicated to processing innocuous and noxious input, manifesting itself as increased readiness of the pain matrix for activation by even innocuous input. Activation of the amygdala in our TMD group could reflect the establishment of aversive associations with tactile stimulation due to the persistence of pain.     

The Role of Blood Osmolality and Volume in Regulating Vasopressin Secretion in the Rat

A sensitive and specific radioimmunoassay for plasma arginine vasopressin (AVP) has been used to study the effects of blood osmolality and volume in regulating AVP secretion in unanesthetized rats. Under basal conditions, plasma AVP and osmolality were relatively constant, averaging 2.3+/-0.9 (SD) pg/ml and 294+/-1.4 mosmol/kg, respectively. Fluid restriction, which increased osmolality and decreased volume, resulted in a progressive rise in plasma AVP to about 10 times basal levels after 96 h. A 2-3-fold increase in plasma AVP occurred as early as 12 h, when osmolality and volume had each changed by less than 2%. Intraperitoneal injections of hypertonic saline, which had no effect on blood volume, also produced a rise in plasma AVP that was linearly correlated with the rise in osmolality (r > 0.9) and quantitatively similar to that found during fluid restriction (plasma AVP increased 2-4-fold with each 1% increase in osmolality). Intraperitoneal injection of polyethylene glycol, which decreased blood volume without altering osmolality, also increased plasma AVP but this response followed an exponential pattern and did not become significant until volume had decreased by 8% or more. At these levels of hypovolemia, the osmoregulatory system continued to function but showed a lower threshold and increase sensitivity to osmotic stimulation. We conclude that AVP secretion is regulated principally by blood osmolality but that the responsiveness of this mechanism may be significantly altered by modest changes in blood volume.     

Acute Renal Failure after Folate: NaKATPase in Isolated Rat Renal Tubule

Abstract. Using refinements of quantitative histochemistry, i.e. oil-well technique, enzymatic Pi analysis and NADP/ NADPH cycling, the activity of NaKATPase (E.C. 3.6.1.3), an enzyme involved in transmembrane ion transport, was measured in single dissected segments of the proximal and distal tubule of male rats 10 min., 30 min., 60 h and 14 days after folate administration (250 mg/kg body weight). 10 min. after injection the onset of acute renal failure was already apparent by an increase in blood urea of 45 per cent and cessation of urine flow. 60 h after folate the rats became polyuric. The kidney wet weight rose by 40 per cent in a few minutes after the injection due to universal tubular dilatation. During the first hours numerous folate casts were localized, mainly in the thick ascending iimb of Henle's loops. In addition precipitates were found intracellularly in the distal part of the proximal convoluted tubules. The straight portion of the proximal tubules was free of precipitates. 10 min. after the injection tubular segments containing folate material did not show Na K ATPase activity, whereas the folate free tubular segments revealed a residual activity of 30 per cent. Only 15 per cent of the tubules within one lyophilized section had collapsed proximal portions with control activity values. However, the less collapsed segments of the distal tubules revealed a loss of Na K ATPase activity of 55 per cent. Thus folate seems to affect the distal tubule first of all. 60 h after folate administration, when kidney growth reached its maximum, the whole nephron lost its Na K ATPase activity. No tubular cell degeneration or necrosis could be detected during the development stage or the sustained phase of renal failure. After addition of folate to renal homogenate, Na K ATPase exhibited activation (+ 35 per cent) and inhibition (–42 per cent and more) of activity plotted against folate concentration. A careful evaluation of the available evidence led to the conclusion that the acute renal failure induced by folate differs markedly from other models by a directly altered tubular cell metabolism in the development stage of oliguria. Acute tubular obstruction may initiate oliguria. However it seems unlikely that tubular obstruction will be the unique pathogenic factor for this syndrome, especially for the development of the tremendous kidney growth. The inhibition of tubular Na K ATPase activity after folate may indicate an impaired tubular active reabsorption capacity which would be involved in the acute renal failure. The most important finding is that glomerular filtration does not seem to be a primary factor in the development of oliguria after folate administration.     

超声对正常人胆管末段及乳头部的测量

目的：完善肝外胆管测量标准,提高下段胆管及壶腹乳头部病变的超声显示率及壶腹周围癌早期诊断率。方法：采用充盈胃、十二指肠,以胰头及肝脏为超声窗,利用横、纵旋转扫查法显示下段胆管。测量７８例正常人胰头段（Ｃ３）及末段（Ｃ４）胆管的内径并观察乳头部的显示状况。结果：应用横旋转扫查法Ｃ３、Ｃ４段胆管显示率分别为８７％、７６％,正常值为３．５９±０．９１ｍｍ、１．９７±０．５１ｍｍ,有４４例（５６％）乳头部得以显示。纵旋转扫查法显示率为７８％、４７％,正常值为３．５７±０．７８ｍｍ、１．９９±０．３９ｍｍ,乳头部显示仅达８％（６例）。不同年龄组测值存在统计学差异,５０岁以上成人较宽。横旋转扫查法明显优于纵旋转法,两者正常值无统计学差异。乳头部声像图表现为胆管、十二指肠开口处壁稍增厚,回声增强之小鱼唇状结构。结论：横旋转扫查法对Ｃ３、Ｃ４段胆管及乳头部的显示率高于纵旋转扫查法,是显示末段胆管较为理想的方法。Ｃ３、Ｃ４段胆管正常值测量及乳头部的显示,将提高超声对该部位病变的早期诊断率,具有重要临床意义     

The Handling of Immunoreactive Vasopressin by the Isolated Perfused Rat Kidney

Using the isolated rat kidney perfused with an artificial medium containing glucose as the sole fuel, we studied the renal handling of immunoreactive arginine vasopressin (AVP) and determined the effect of various factors on the ability of the kidney to remove AVP.     

肾集合管癌1例报告并文献复习

目的：探讨起源于肾髓质集合管的肾集合管癌,分析其病理形态学特征及鉴别诊断.方法：对3例肾集合管癌进行大体,光镜及免疫组化观察并结合文献复习.结果：肿瘤主要位于肾髓质,囊实性肿块,呈灰白或灰黄色,侵袭性强;镜下肿瘤呈弥漫性或腺管状,乳头状排列,肿瘤间质纤维组织反应性增生,多量浆细胞或淋巴细胞浸润;免疫组化：CK（AE3） 、EMA .vimentin（＋）,CD10、CEA、CK7和CK20（-） .结论：肾集合管癌是一种起源于肾髓质集合管的罕见性肾肿瘤,恶性度高,预后差,确诊本病时应与肾乳头状癌和肾髓质癌鉴别.     

On the Mechanism of Inhibition in Fluid Reabsorption by the Renal Proximal Tubule of the Volume-Expanded Rat

We undertook to determine the extent to which the inhibition in absolute proximal fluid reabsorption in response to expansion of extracellular volume with noncolloid-containing solutions is the result of concomitant reductions in postglomerular (efferent arteriolar) protein concentration. Selective elevation of efferent arteriolar oncotic pressure in volume-expanded rats (Ringer's 10% body weight) to levels slightly in excess of normal by microperfusion with 9-10% albumin-Ringer's solution nearly completely reversed the inhibition in absolute and fractional reabsorption in adjacent proximal tubules. In contrast, during similar microperfusion with a 6-7% albumin solution, no increase in proximal reabsorption was measured. We interpret these findings to indicate that the bulk of the inhibition in absolute proximal reabsorption in response to volume expansion with colloid-free solutions is causally mediated by the accompanying parallel decline in postglomerular vascular protein concentration.