Net Sodium Transport Research Articles

Impacts of vertically propagating tides on the mean state of the ionosphere‐thermosphere system

The National Center for Atmospheric Research Thermosphere‐Ionosphere‐Electrodynamics General Circulation Model (TIE‐GCM) is utilized to understand the role that upward propagating tides play in determining the zonal mean state of the ionosphere‐thermosphere system. A sensitivity assessment of the TIE‐GCM shows that TIE‐GCM solutions greatly depend on the lower boundary conditions. We also establish the veracity of our TIE‐GCM solutions within and above the dynamo region. To isolate the mean effects of tidal dissipation, differences between TIE‐GCM simulations with and without lower boundary tidal forcing as specified by the Climatological Tidal Model of the Thermosphere are investigated. Dissipation of the DW1, (diurnal westward propagating tide with zonal wave number 1), diurnal eastward propagating tide with zonal wave number 3, and SW2 (semidiurnal tide with zonal wave number 2) explains most of ∼10–30 m s−1 seasonal and latitudinal variability in zonal winds within the dynamo region, with SW2 playing a greater role than ascribed in previous studies. Tidal dissipation at low latitudes causes a 9% decrease (30% increase) in [O] ([O2]) number densities near the F2 layer peak, leading to at least a 9% decrease in peak electron density (NmF2) throughout the year. F2 layer peak height (hmF2) differences of ‐4 to 2 km at low latitudes are explained by variations in the field‐aligned plasma motion driven by meridional wind differences induced by tidal dissipation. Compositional effects are mainly driven by DW1 and SW2, which differs from previous interpretations of tidal‐driven composition changes by DW1 “tidal mixing” exclusively. We suggest that tides may produce a net transport of constituents in the thermosphere similar to the way that, e.g., gravity waves can drive net transport of sodium in the mesosphere.

Hydration status affects sodium, potassium, and chloride transport across rat urothelia

Recent data suggest possible net transport of urinary constituents across mammalian urinary tract epithelia (urothelia). To evaluate the effect of animal hydration status on such transport, we instilled urine collected during 2-day water deprivation, water loading, or ad libitum water intake into isolated in situ bladder(s) of groups of rats undergoing one of the same three hydration states. After 1-h bladder dwell, we retrieved the urine and measured differences in volume and solute concentrations between instilled and retrieved urine. We previously reported results regarding changes in urine volume and net urea and creatinine transport and herein report the results of net urinary sodium, potassium, and chloride transport in the same animals. During water-loading conditions, urinary concentrations of Na, K, and Cl rose 4.9 (30.7%), 2.6 (16.5%), and 6.0 meq/l (26.8%), respectively, indicating urothelial secretion into urine. During ad libitum water intake, urinary K and Cl concentrations fell 33.6 (14.8%) and 28.4 meq/l (12%), respectively (Na did not change), and during water deprivation urine Na, K, and Cl concentrations fell dramatically by 53.2 (18.6%), 159.4 (34.6%) and 133.7 meq/l (33.8%), respectively, reflecting urothelial reabsorption of each ion. For each ionic species, two factors independently influenced transport: instilled urinary ion concentration and animal hydration state. These results demonstrate significant regulated ion transport across mammalian urothelia, support the notion that lower urinary tract modifies final urine, and suggest that the lower urinary tract may play a role in local and whole animal solute homeostasis.

Angiotensin II rapidly stimulates the short‐circuit current in opossum kidney cells expressing rat Na,K‐ATPase

The binding of angiotensin II (Ang II) to the angiotensin receptor (AT1) stimulates Na,K‐ATPase activity that drives sodium reabsorption in the proximal tubule, which reabsorbs 2/3 of the filtered sodium. To determine how quickly Ang II can stimulate Na,K‐ATPase in the proximal tubule, the α‐1 subunit of rat kidney Na,K‐ATPase and the AT1a receptor were stably co‐expressed in opossum kidney cells. Cells were grown on permeable supports and mounted in an Ussing Chamber containing Ringer's solution. The addition of 10 μM Ang II to the basolateral side increased the short‐circuit current (Isc), which is proportional to net sodium transport, in ≤ ~10 sec. Isc peaked at ~20 sec and declined to a plateau above baseline for over 3 min. The subsequent addition of 200 μM nystatin to increase the sodium permeability of the apical membrane, and thereby the concentration of intracellular sodium, increased Isc to the level of the Ang II‐dependent peak. Subsequently adding 600 μM ouabain, which inhibits Na,K‐ATPase, reduced Isc to its original baseline value. Thus, Ang II significantly stimulated Na,K‐ATPase activity and transcellular sodium transport in 10 seconds or less. We hypothesize that such rapid Ang II‐dependent stimulation of sodium reabsorption in the proximal tubule is part of a mechanism to help the body to recover from a sudden drop in blood pressure. Supported in part by HL096800 to F.S.

Na+-independent transport of bipolar and cationic amino acids across the luminal membrane of the small intestine.

The role of sodium in transport of bipolar and cationic amino acids and their interactions were examined in vitro by measuring unidirectional influx across the brush-border membrane of intact rat jejunal and rabbit ileal epithelia. The chloride-dependent and beta-alanine inhibitable B(0,+) present in rabbit ileum was blocked by combining inhibition by beta-alanine with Na(+)- or Cl(-)-free conditions. Under these conditions, lysine influx across the brush-border membrane is Na+ independent. All Na+-independent influx of cationic and bipolar amino acids is by a system b(0,+) equivalent in the brush-border membrane of both species, where a system y+ is not present. System b(0,+) is shown to be a potent exchanger of intracellular leucine for extracellular lysine and of intracellular lysine for extracellular leucine. The model used to explain leucine stimulation of mucosa to serosa lysine transport can explain Na+ dependence of net lysine absorption. On the assumption that b(0,+) in situ, like the transporter induced by retroperitoneal brown adipose tissue in Xenopus laevi oocytes, acts as an obligatory exchanger, this model can also explain the effects of lysine on short-circuit current and net transport of sodium and the effect on transport capacity by preincubation at Na+-free conditions.

Lactate transport across the bovine rumen epithelium in vitro.

The in vitro transport of L-lactate across rumen epithelium was found to be a passive, mass-action regulated diffusion, and no saturable transport mechanisms were involved at concentrations from 2-20 mmol/L. During this increase in L-lactate concentrations the epithelial resistance and potential difference increased significantly, indicating an epithelial change towards a more tight epithelium. The net sodium transport was significantly reduced by 45% at 20 mmol/L lactate as compared to lactate free conditions.

Sodium transport across the caecal and colonic epithelium of germfree and specific-pathogen free rats.

It was assumed that the enlarged caecum and the accumulation of semiliquid contents in germfree rats is accompanied by changes in sodium absorption. Transepithelial sodium fluxes were studied under Ussing chamber conditions across epithelial sheets of the caecum and colon of germfree (GF) and specific-pathogen free (SPF) rats. Net sodium transport was highest in the proximal colon and in the proximal segment of the distal colon; it was considerably lower in the caecum and in the distal segment of the distal colon. In the caecum and proximal colon of the GF rats, the electroneutral sodium absorption was increased as compared to the SPF rats. In the proximal segments of the distal colon, no differences were seen. In the distal segment of the distal colon, the mainly electroneutral sodium transport in the SPF rats was changed into electrogenic transport in the GF rats. These differences may be due to the increased aldosterone levels of the GF rats.

Transport of sodium across the isolated bovine rumen epithelium: interaction with short-chain fatty acids, chloride and bicarbonate.

Unidirectional transport rates of sodium (22Na+) and chloride (36Cl-) across bovine rumen epithelium were measured in vitro by the Ussing chamber technique. The active and short-chain fatty acid (SCFA)-stimulated sodium transport was shown to fit Michaelis-Menten kinetics, and was rate limited mainly by one transport system, characterized by a Km of 43 mmol l-1 Na+ and a Jmax (maximal transport rate) of 6.2 mumol cm-2 h-1 Na+. It was confirmed that the basolateral Na+,K(+)-ATPase was essential for active sodium transport, and that an apical amiloride-sensitive sodium transport system (Na(+)-H+ exchange) was involved in a minimum of 60-70% of the active sodium transport in the presence of SCFAs (butyrate). The main part of both the mucosal-serosal (MS) and serosal-mucosal (SM) sodium flux was sensitive to an applied electrical potential difference (PD). It is noteworthy that an applied PD, equal to the in vivo PD (+30 mV, lumen as reference), abolished net transport of sodium. The stimulating effect of a mixture of acetate, propionate and butyrate on active sodium transport was confirmed, and it was further shown that the stimulating effect of each of the three SCFAs was nearly equal. Analogues of naturally occurring SCFAs (isobutyrate and 2-ethyl-butyrate) did not stimulate active sodium transport, but inhibited the stimulating effect of butyrate. The stimulating effect of butyrate was clearly concentration dependent and showed a maximum at approximately 20 mmol l-1 butyrate. Above this limit active sodium transport was decreased with increasing butyrate concentration. This suggests that there was a limit to the amount of butyrate that could be handled by the epithelium. The active sodium transport was clearly correlated with the chloride concentration, and was significantly reduced, but not abolished, by replacement of chloride with gluconate. Active transport of chloride was stimulated by butyrate and reduced by the Na(+)-H+ exchange inhibitor amiloride (3 mmol l-1). There was no effect of the Cl(-)-HCO3- exchange inhibitor DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid; 0.5 mmol l-1) on sodium transport. HCO3- (13 mmol l-1) and CO2 (5%) themselves had only a small and non-significant stimulating effect on sodium fluxes, however, in the presence, but not the absence of HCO3- and CO2 in the experimental solutions acetazolamide (1 mmol l-1) significantly reduced active sodium transport. It is concluded that SCFAs could stimulate the active sodium and chloride transport as a result of their metabolism. The CO2 produced could stimulate apical Na(+)-H+ and Cl(-)-HCO3- exchangers running in parallel via increased H+ and HCO3- gradients.

Evidence for apical Na+/H+ exchanger in bovine main pancreatic duct.

The finding of a high PCO2 in basally secreted pancreatic juice of man and dog raises the hypothesis of proton secretion from ductal epithelial cells presumably through a Na+/H+ exchanger. To test this possibility, H+ luminal secretion and Na+ movements were measured in vitro on samples of bovine pancreatic ducts mounted in Ussing-type chambers. The rate of luminal acidification measured by the pH stat method, using bicarbonate-free media gassed with 100% O2, reached 2.75 muEq/cm2/hr. Proton secretion was blocked in the presence of 1 nM amiloride or in the absence of Na+ (replaced by choline) in the mucosal solution. Study of transepithelial 22Na fluxes in short-circuited tissue, bathed on both sides by control Ringer solution, gassed by 95% O2-5% CO2 demonstrated a net sodium transport from the mucosal to the interstitial side of the duct (net 22Na flux = 3.23 +/- 0.8 muEq/cm2/hr). This net sodium transport was electroneutral and blocked by mucosal amiloride (0.5-1 mM/liter) or by interstitial ouabain (1 mM/liter). These results are consistent with the existence of a Na+/H+ exchanger on the luminal side of the bovine main pancreatic duct.

Parathyroid Hormone Stimulates Electrogenic Sodium Transport in A6 Cells

The effects of parathyroid hormone (PTH) on sodium homeostasis in the distal tubule are not well defined. Using A6 cells as a model for distal tubular epithelium we measured equivalent short circuit current (leq), as an estimate of net sodium transport. We found that PTH increased leq in a dose-dependent manner. DDA, an agent which inhibits adenylate cyclase, decreased PTH-activated sodium transport, suggesting a role for cAMP elevation in PTH effects. Moreover, addition of Rp-cAMP, an inhibitor of cAMP-dependent protein kinase, partially blocked the PTH-stimulated leq. PTH also elicited a sustained increase in [Ca2+]i in A6 cells. This elevation in [Ca2+]i was abolished by removal of calcium from the extracellular medium, suggesting the involvement of calcium influx pathways. In fact, addition of the calcium channel blocker nitrendipine to PTH-stimulated leq partially blocked PTH-activated sodium transport. Taken together these data demonstrate that PTH stimulates electrogenic sodium transport in A6 cells and that this effect may be mediated through a rise in both intracellular calcium and cellular cAMP.

Regulation of Airway Surface Liquid on the Isolated Guinea-pig Trachea

Summary: Isolated guinea-pig tracheae exposed to conditioned air mucosally and to circulating saline solutions serosally have been subjected to an osmotic gradient between saline and airway surface and to a range of drugs. Experiments were conducted to examine the mechanisms that regulate airway surface liquid during condensation and evaporation. Measurements were made of the depth of airway surface liquid, its sodium activity, the transepithelial potential difference, and of net water and sodium transport across the airway. Results suggest that osmotic gradients have profound effects on airway surface liquid but drugs that influence secretory activity (methacholine, substance P) or ion transport activity (amiloride, bumetanide, oubain) do not.

ACTIVATION AND PHYSIOLOGICAL ROLE OF Na+/H+ EXCHANGE IN LAMPREY (LAMPETRA FLUVIATILIS) ERYTHROCYTES

The effects of intracellular acidification, osmotic shrinkage and ss-adrenergic stimulation on sodium transport across the membrane of lamprey (Lampetra fluviatilis) erythrocytes were investigated. Unidirectional ouabain-insensitive sodium flux, measured using radioactive 22Na, was increased markedly by intracellular acidification, to a lesser extent by osmotic shrinkage and only modestly by ss-adrenergic stimulation. Na+/H+ exchange was activated in all of these cases. However, net sodium influx (and cell swelling caused by the influx of osmotically obliged water) was seen only in cells subjected to intracellular acidification. In contrast, practically no changes in red cell pH or in water or ion (Na+, K+ and Cl-) contents were seen after osmotic shrinkage or ss-adrenergic stimulation. Calculations of the [Na+]o/[Na+]i and [H+]o/[H+]i ratios across the erythrocyte membrane suggest that the virtual lack of net sodium movements in osmotically shrunken erythrocytes is due to the absence of a driving force for net transport of these ions via the Na+/H+ exchange pathway. It also appears that, in physiological conditions, the increase in the activity of the Na+/H+ exchanger by ss-adrenergic stimulation is too small to mediate detectable net sodium transport.

Evaporation-induced changes in airway surface liquid on an isolated guinea pig trachea.

An isolated preparation of the guinea pig trachea was developed. The trachea was exposed serosally to Krebs-Henseleit solution and mucosally to tidal airflow, designed to mimic conditions in vivo. The preparation establishes stable layers of airway surface liquid (ASL). Typical depth, transepithelial potential differences, and sodium activity are 200 microns, -3 mV, and 125 mM, respectively (approximate sodium concn 170 mM). When exposed to air with a vapor pressure deficit (VPD), evaporation of water occurs from ASL, ASL depth decreases, and the concentration of sodium ions in ASL increases. The water content of air passing over the trachea also increases. This measurement is compared with measurements of the change in volume of ASL, based on depth changes, to yield estimates of net water transport (NWT). Measurements of changes in the sodium content of ASL allow for the calculation of net sodium transport by the trachea. Evaporation rate, changes in the volume of ASL, NWT, and net sodium transport are all influenced by VPD. The results suggest that evaporation from ASL increases its sodium concentration (and osmotic pressure) and increases osmotically driven NWT to replace water lost. Evaporation-induced increases in the sodium concentration appear to be limited by enhanced sodium uptake at high VPD.

Intestinal transport of sodium, glucose and immunoglobulin in neonatal pigs. Effect of glucocorticoids.

The effect of cortisol on plasma immunoglobulin G (IgG) levels and on jejunal transport of sodium and glucose has been investigated in neonatal pigs (0-7 days of age). Five pigs were delivered vaginally (VD) at term (114-115 days gestation) and thirty-five by caesarean section (CS) 2-4 days before term (to circumvent a neonatal cortisol surge). Postnatally, twenty-seven CS pigs were injected with adrenocorticotrophic hormone (ACTH; n = 13), metyrapone (an inhibitor of adrenal 11 beta-hydroxylase activity, n = 7) or physiological saline (n = 7). Pigs were killed at birth, at 3 days, or at 6-7 days of age. Plasma concentrations of cortisol and IgG were determined and unidirectional fluxes of sodium and glucose measured across the proximal jejunum in vitro. Newborn CS pigs had significantly lower plasma cortisol but higher net fluxes of sodium and glucose than newborn VD pigs. At 3-7 days, metyrapone-treated pigs had significantly lower concentrations of cortisol and IgG in plasma and lower net fluxes of sodium and glucose than ACTH-treated pigs. Differences in net fluxes between treatment groups resulted from changes in both electrogenic and non-electrogenic sodium transport. Furthermore, sodium-glucose co-transport accounted for a major proportion of net sodium transport. High unidirectional fluxes in newborn CS pigs may be explained by the passage of large amounts of sodium through tight junctions and paracellular pathways in the prepartum period. The results indicate that cortisol stimulates net transport of sodium, glucose and immunoglobulins in the postnatal period of caesarean-delivered pigs. However, cortisol is unlikely to play a major regulatory role in the postnatal maturation of intestinal transport in normally delivered pigs.

Deficiency of red cell sodium-potassium pump activity in bipolar affective disorder

The rat proximal tubule epithelium is represented as well-stirred, compliant cellular and paracellular compartments bounded by mucosal and serosal bathing solutions. With a uniform pCO2 throughout the epithelium, the model variables include the concentrations of Na, K, Cl, HCO3, H2PO4, HPO4, and H, as well as hydrostatic pressure and electrical potential. Except for a metabolically driven Na-K exchanger at the basolateral cell membrane, all membrane transport within the epithelium is passive and is represented by the linear equations of nonequilibrium thermodynamics. In particular, this includes the cotransport of Na-Cl and Na-H2PO4 and countertransport of Na-H at the apical cell membrane. Experimental constraints on the choice of ionic conductivities are satisfied by allowing K-Cl cotransport at the basolateral membrane. The model equations include those for mass balance of the nonreacting species, as well as chemical equilibrium for the acidification reactions. Time-dependent terms are retained to permit the study of transient phenomena. In the steady state the energy dissipation is computed and verified equal to the sum of input from the Na-K exchanger plus the Gibbs free energy of mass addition to the system. The parameter dependence of coupled water transport is studied and shown to be consistent with the predictions of previous analytical models of the lateral intercellular space. Water transport in the presence of an end-proximal (HCO3-depleted) luminal solution is investigated. Here the lower permeability and higher reflection coefficient of HCO3 enhance net sodium and water transport. Due to enhanced flux across the tight junction, this process may permit proximal tubule Na transport to proceed with diminished energy dissipation.

Mechanism of electrically silent Na and Cl transport across the rumen epithelium of sheep

This study was designed to study the mechanism of electroneutral Na and Cl transport across the isolated rumen epithelium of sheep. Net sodium transport (5.75 +/- 0.35 microequiv cm-2 h-1) was significantly higher than the short-circuit current (0.95 +/- 0.08 microequiv cm-2 h-1). Both, net sodium and net chloride transport were markedly reduced by replacement of chloride, bicarbonate and sodium, respectively, but were not changed by the absence of mucosal potassium. Net sodium and net chloride absorption was significantly decreased by 1.0 mM-amiloride. Mucosal addition of bumetanide, furosemide, hydrochlorothiazide or low concentrations of amiloride (less than 0.1 mM) did not change sodium fluxes. These results provide compelling evidence consistent with the presence of Na-H exchange as the predominant electroneutral mechanism for transepithelial sodium movement. The ion replacement studies and data from literature suggest that the Na-H exchange is working in parallel with a Cl-HCO3 exchange although luminal addition of DIDS (4,4'diisothiocyanatostilbene-2,2'-disulphonate, 1 mM) did not significantly influence Cl transport.

Regulation of the amiloride-blockable sodium channel from epithelial tissue

The first step in net active transepithelial transport of sodium in tight epithelia is mediated by the amiloride-blockable sodium channel in the apical membrane. This sodium channel is the primary site for discretionary control of total body sodium and, therefore, investigating its regulatory mechanisms is important to our understanding of the physiology of fluid and electrolyte balance. Because essentially all of the regulatory sites on the channel are on the intracellular surface, patch clamp methods have proven extremely useful in the electrophysiological characterization of the sodium channel by isolating it from other channel proteins in the epithelial membrane and by allowing access to the intracellular surface of the protein. We have examined three different regulatory mechanisms. (1) Inhibition of channel activity by activation of protein kinase C; (2) activation of the channel by agents which activate G-proteins; and (3) modulation of channel kinetics and channel number by mineralocorticoids. Activation of protein kinase C by phorbol esters or synthetic diacylglycerols reduces the open probability of sodium channels. Protein kinase C can be activated in a physiological context by enhancing apical sodium entry. Actions which reduce sodium entry (low luminal sodium concentrations or the apical application of amiloride) increase channel open probability. The link between sodium entry and activation of protein kinase C appears to be mediated by intracellular calcium activity linked to sodium via a sodium/calcium exchange system. Thus, the intracellular sodium concentration is coupled to sodium entry in a negative feedback loop which promotes constant total entry of sodium. Activation of G-proteins by pertussis toxin greatly increases the open probability of sodium channels. Since channels can also be activated by pertussis toxin or GTP gamma S in excised patches, the G-protein appears to be closely linked in the apical membrane to the sodium channel protein itself. The mechanism for activation of this apical G-protein, when most hormonal and transmitter receptors are physically located on the basolateral membrane, is unclear. Mineralocorticoids such as aldosterone have at least two distinct effects. First, as expected, increasing levels of aldosterone increase the density of functional channels detectable in the apical membrane. Second, contrary to expectations, application of aldosterone increases the open probability of sodium channels. Thus aldosterone promotes the functional appearance of new sodium channels and promotes increased sodium entry through both new and pre-existant channels.

Inhibition by loperamide of mucus secretion in the rat colon in vivo

The effect of loperamide on mucus secretion and the net transport of fluid, sodium and potassium was investigated in the perfused rat colon in vivo. Prostaglandin E 2 (PGE 2, 1 mg/kg per h intraarterially) and deoxycholic acid (2 mM intraluminally) were used as secretagogues. Mucus secretion was determined as the total amount of protein-bound hexose in the effluent. Under basal conditions, loperamide (6 mg/kg subcutaneously) slightly decreased mucus secretion and increased the absorption of fluid and sodium. PGE 2 and deoxycholic acid stimulated mucus secretion about 4- and 9-fold, respectively. Loperamide abolished the mucus secretory response to PGE 2 and reduced the response to deoxycholic acid by 50%. It also reduced the fluid secretion following PGE 2 but did not affect the diminished fluid absorption following deoxycholic acid. Potassium secretion was not significantly influenced by loperamide and therefore was independent of the secretion of mucus. The data suggest that loperamide is a potent inhibitor of colonic mucus secretion, a property that possibly contributes to the antidiarrheal effect of this opiate analogue.

The effects of lithogenic bile on gallbladder epithelium.

Prairie dogs were fed a 1.2% cholesterol diet for up to 24 weeks to evaluate the effects of lithogenic bile on the mucosa of the gallbladder. There was a progressive increase in the lithogenic index of the gallbladder bile (1.44 +/- 0.15 at 4 weeks, p less than 0.05). Fifty-five of 70 animals developed gallstones between the second and fourth week. Increasing stone burden was associated with a 27% (p less than 0.05) decrease in the electrical resistance of the epithelium and a 60% (p less than 0.05) decrease in net sodium transport when measured isotopically in an Ussing chamber (3 weeks). After 4 months, seven of ten animals developed inflammatory mucosal polyps characterized by a heavy infiltration of plasma cells into an expanded matrix. Cellular infiltration began as early as 2 weeks. These changes occurred without alterations in the ultrastructural appearance of the epithelium.

Tonic activity of submucosal neurons influences basal ion transport

The influence of tonically active submucosal neurons on basal ion transport was studied using sheets of guinea pig ileum set up in flux chambers. Tetrodotoxin evoked an immediate and sustained decrease in short-circuit current that was sustained for 60 minutes compared with control tissues in which basal currents gradually decreased over time. Time-dependent changes in basal short-circuit currents in tissues treated with atropine were not significantly different from control tissues. The decrease in short-circuit current after tetrodotoxin resulted from a greater increase in net chloride absorption than sodium absorption. Changes in net sodium and chloride transport were due to an increase in the mucosal-to-serosal fluxes of these ions. The results suggest that tonic activity of submucosal neurons limits the absorptive capacity of the guinea pig ileum.

Effects of kinin on electrolytes transport and regulation of kininase activity in distal nephron segments of the rat.

It is generally recognized that the cortical collecting duct plays a major role in the fine control of renal sodium excretion, and thus in the regulation of extracellular fluid volume. Several lines of evidence point to the cortical collecting duct as a possible site of kinin action on sodium transport. First, both kallikrein1-3 and kininogen4 have been localized to the collecting duct system. Second, high-affinity binding sites for bradykinin have recently been localized to the cortical and outer medullary collecting ducts5. Third, kinins have a marked inhibitory effect on vasopressin-stimulated water permeability in the isolated, perfused cortical collecting duct of the rabbit. First part of our studies is to investigate whether bradykinin directly affects net sodium transport in the cortical collecting duct of the rat using the isolated, perfused tubule technique.KeywordsSodium TransportDistal NephronNeutral EndopeptidaseElectrolyte TransportCortical Collect DuctThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.