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PubMed1994

Nitric oxide involvement in sodium choleate-induced fluid secretion and diarrhoea in rats.

Bile salt-induced diarrhoea, net water and electrolyte secretion, gastrointestinal transit and nitric oxide (NO) synthase activity were studied in rats. NG-Nitro-L-arginine methyl ester (2.5-25 mg/kg i.p.), an inhibitor of NO synthase, and dexamethasone (0.03-0.3 mg/kg i.p.), an inhibitor of the inducible isoform of NO synthase, antagonized the diarrhoeal response. The NO precursor, L-arginine and isosorbide-5-mononitrate (an NO donor), reversed the inhibitory effect of NG-nitro-L-arginine methyl ester. The bile salt-stimulated fluid secretion, transit through the gut and NO synthase all were inhibited by NG-nitro-L-arginine methyl ester (but not NG-nitro-D-arginine methyl ester). NO synthase activity also was inhibited by dexamethasone. The results are consistent with bile salt induction of epithelial cell injury and concomitant synthesis of NO, mainly through activation of the inducible form of the enzyme. We believe that in this study NO is a mediator of intestinal secretion and motility changes that enhance transit of luminal contents through the gut, resulting in diarrhoea.

Amino Acid Oxidoreductases↗

PubMed1992

Amblyomma americanum (L.): protein kinase C-independent fluid secretion by isolated salivary glands.

Protein kinase C activity was partially purified from tick salivary glands by fast protein liquid chromatography anion-exchange chromatography. Enzyme activity was stimulated by Ca2+, phosphatidylserine, and diacylglycerol with the highest activity observed in the presence of all three modulators. Enzyme activity was inhibited by a synthetic pseudosubstrate peptide with an amino acid sequence resembling the protein kinase C substrate phosphorylation site. The protein kinase C activator, 1-oleoyl-2-acetyl-sn-glycerol (OAG), when added to whole in vitro salivary glands previously prelabeled with 32P, stimulated the phosphorylation of salivary gland proteins. Activators of protein kinase C (phorbol ester or OAG) did not stimulate fluid secretion by isolated tick salivary glands. OAG and phorbol ester had only minimal affects on the ability of dopamine to stimulate secretion by isolated salivary glands and dopamine's ability to increase salivary gland cyclic AMP.

Amino Acid Sequence↗

PubMed1984

Neurotensin increases net fluid secretion and transit rate in the small intestine of man.

In a double-blind study with six patients, who previously had undergone proctocolectomy for ulcerative colitis, the ileostomy discharge significantly increased from 110 to 295 ml X 4 h-1 during infusion of neurotensin, 3 pmol X kg-1 X min-1 for 4 h. Transit defined as the passage of a perorally ingested unabsorbable marker (polyethylene glycol, PEG 4000) was significantly increased during the last hour of neurotensin infusion. The dose of neurotensin used in this study has previously been shown to result in plasma levels of neurotensin-like immunoreactivity within the range obtained after a fatty meal. Thus, the present data indicate that neurotensin in man may exert a physiological function by increasing net fluid secretion in the small intestine as well as increasing the intestinal transit rate.

Adult↗

PubMed1993

Reversal by short-chain fatty acids of colonic fluid secretion induced by enteral feeding.

Diarrhoea complicates enteral feeding in up to 25% of patients. In-vivo perfusion studies in healthy subjects have shown secretion of salt and water in the ascending colon in response to enteral feeding. This study investigated the effect of short-chain fatty acids (SCFA) on this secretory response. Six healthy volunteers underwent segmental in-vivo colonic perfusion. First, baseline fasting colonic water and electrolyte movement was established, then a standard polymeric enteral diet was infused into the stomach while the colon was perfused with either a control electrolyte solution or a test solution containing SCFA. The electrolyte concentrations and osmolality of the two perfusates were identical. In the fasting state water was absorbed throughout the colon. During the control infusion there was significant (p < 0.05) secretion of water in the ascending colon (median rate 1.0 mL per min [95% CI 2.8 mL per min secretion to 0.8 mL per min absorption]). During the SCFA infusion the secretion was significantly reversed (p < 0.05) and there was net absorption (1.6 [0.8-3.7] mL per min). In the distal colon water absorption was significantly greater during the control infusion than during fasting (3.7 [2.5-4.6] vs 1.3 [0.3-2.2] mL per min); during the test infusion this absorption persisted (2.8 [1.3-3.6] mL per min). Movement of sodium, chloride, and potassium ions was similar to that of water in all stages of the study. Bicarbonate movement did not significantly change at any stage. Infusion of SCFA directly into the caecum reverses the fluid secretion seen in the ascending colon during enteral feeding. This finding could have implications for the management of diarrhoea related to enteral feeding.

Adult↗

PubMed2005

Expression of aquaporin-5 in and fluid secretion from immortalized human salivary gland ductal cells by treatment with 5-aza-2'-deoxycytidine: a possibility for improvement of xerostomia in patients with Sjögren's syndrome.

The aim of the present study was to investigate the possibility that ductal cells, which preferentially survive and/or proliferate in Sjögren's syndrome (SS) salivary glands of patients with SS, could acquire the functional expression of membrane water channel aquaporin-5 (AQP5). Thus, in this study, we demonstrate that an immortalized normal human salivary gland ductal cell (NS-SV-DC) line, lacking the expression of AQP5, acquires AQP5 gene expression in response to treatment with 5-aza-2'-deoxycytidine (5-Aza-CdR), a DNA demethylating agent. Confocal microscopic analysis revealed the localization of AQP5 expression mainly at the apical and lateral sides of the plasma membrane. The expressed AQP5 protein was functionally active because AQP5 expression resulted in a significant increase in the osmotically directed net fluid rate across monolayers of NS-SV-DC cells. By the analysis of bisulfite sequencing of CpG islands in the AQP5 promoter, hypermethylation within the consensus Sp1-binding sites was commonly observed in parental cell clones, whereas demethylation at the CGs, one in the second consensus Sp1 element and the other outside of the third consensus Sp1 element in the AQP5 promoter, was detected in NS-SV-DC cells after treatment with 5-Aza-CdR. By analyzing the luciferase activity of transfected AQP5 promoter vectors, it became evident that demethylation at the CGs cooperatively functions between these two sites to induce AQP5 expression. Our data, therefore, suggest that treatment of ductal cells with 5-Aza-CdR could result in the expression of the AQP5 gene, thereby leading to increased fluid secretion from ductal cells in SS salivary glands.

Aquaporin 5↗

PubMed1994

Seminiferous tubule fluid secretion is a Sertoli cell microtubule-dependent process inhibited by 2,5-hexanedione exposure.

Mammalian Sertoli cells are responsible for the formation and secretion of seminiferous tubule fluid (STF) which provides the nutritional and hormonal microenvironment necessary for spermatogenesis. Exposure of rats to 2,5-hexanedione (2,5-HD) results in testicular injury characterized by a decrease of STF secretion which immediately precedes bulk germ cell necrosis. The earliest biochemical change in 2,5-HD-exposed rats is an alteration in testicular microtubule assembly kinetics. In this study, we investigate the relationship between microtubule-dependent processes and STF secretion in adult Sprague-Dawley CD rats by exposing seminiferous tubules to two types of toxicants: (1) those which alter microtubules (colchicine and 2,5-HD) and (2) an inhibitor of protein secretion (brefeldin A, [BFA]). Secretion of STF is quantitated by monitoring the rate of transport of a microinjected oil droplet in the lumen of isolated seminiferous tubules using time-lapse stereoscopic microscopy. The rate of oil droplet transport in seminiferous tubules isolated from testis pretreated in vivo for 2 hr with colchicine (40 micrograms/testis) was significantly decreased. Exposure of isolated seminiferous tubules to BFA (10 micrograms/ml) for 40 min also significantly decreased the transport of lumenal oil droplets. Exposure of rats to 1%, 2,5-HD in drinking water decreased transport of injected oil droplets in seminiferous tubules beginning at 3 weeks of exposure in the absence of significant alterations in testicular morphology. These data demonstrate that normal STF secretion requires an intact, microtubule-dependent intracellular membrane transport pathway and strengthen the association between 2,5-HD-induced disruption of Sertoli cell STF secretion and 2,5-HD-induced alterations in Sertoli cell microtubules.

Analysis of Variance↗

PubMed1992

Cl- fluxes related to fluid secretion by the rat parotid: involvement of Cl(-)-HCO3- exchange.

Muscarinic-induced 36Cl- and 86Rb+ (K+ substitute) fluxes were studied in rat parotid acini. Stimulation resulted in a rapid [half time (t1/2) less than 30 s] decrease in both Cl- and Rb+ content (approximately 50 and 30%, respectively) followed by a slower partial recovery (t1/2 approximately 3-4 min) to approximately 80% of resting levels for both ions. Cl- loss was inhibited by the venom of Leiurus quinquestriatus, which contains the maxi-K+ channel blocker charybdotoxin. Cl- recovery was blunted in the presence of bumetanide, an inhibitor of Na(+)-K(+)-Cl- cotransport, or on HCO3- removal and was completely blocked in the presence of bumetanide and 4,4' diisothiocyanostilbene-2,2' disulfonic acid (DIDS), an inhibitor of Cl(-)-HCO3- exchange. In HCO3(-)-containing medium a rapid (t1/2 less than 1 min), DIDS-inhibitable cytoplasmic alkalinization (approximately 0.4 pH unit) was observed in acini switched to a Cl(-)-free solution. This alkalinization was not seen in HCO3(-)-free medium but persisted in the absence of Na+, consistent with the presence of a potent Na(+)-independent Cl(-)-HCO3- exchanger. Kinetic studies indicated that the half-maximal effect of this exchanger for extracellular Cl- was approximately 18 mM. These results are consistent with the hypothesis that secretagogue-induced KCl loss by salivary acinar cells occurs via electrically coupled K+ and Cl- channels. In addition, they provide strong evidence that Cl- entry into, and thus fluid secretion by, these cells is mediated by both Cl(-)-HCO3- exchange and Na(+)-K(+)-Cl- cotransport.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1981

Salivary gland of the tick vector (R. appendiculatus) of East Coast fever. II. Cellular basis for fluid secretion in the type III acinus.

Fluid balance is a major physiological problem for hematophagous ticks. To maintain osmotic balance they must conserve water for prolonged periods while seeking a mammalian host, and they must eliminate a very large volume of excess fluid taken in during a relatively short period of feeding. This is accomplished in part by modification of the salivary gland during 7-10 days of feeding to secrete a copious saliva which is pumped into the bovine host. This function has previously been attributed to certain interstitial epithelial cells of the type III acinus which differentiate in the course of feeding into cells reminiscent of those of the avian salt gland. The ultrastructural changes in the type III acinus during the blood-meal were studied. In addition to the differentiation of the interstitial cells, this paper describes a remarkable sequence of changes in external form and internal organization of the e-cells. This results in their transformation from typical protein-secreting glandular cells to transport cells having myriad basolateral processes interdigitating with those of the ablumenal interstitial cells to form a basal labyrinth comparable to that of other fluid-transporting epithelia. The findings are discussed in relation to various postulated mechanisms for fluid and electrolyte transport.

Animals↗

PubMed1999

Radiation-induced progressive decrease in fluid secretion in rat submandibular glands is related to decreased acinar volume and not impaired calcium signaling.

The mechanism(s) of radiation-induced salivary gland dysfunction is poorly understood. In the present study, we have assessed the secretory function (muscarinic agonist-stimulated saliva flow, intracellular calcium mobilization, Na+/K+/2Cl- cotransport activity) in rat submandibular glands 12 months postirradiation (single dose, 10 Gy). The morphological status of glands from control and irradiated rats was also determined. Pilocarpine-stimulated salivary flow was decreased by 67% at 12 months (but not at 3 months) after irradiation. This was associated with a 47% decrease in the wet weight of the irradiated glands. Histological and morphometric analysis demonstrated that acinar cells were smaller and occupied relatively less volume and convoluted granular tubules were smaller but occupied the same relative volume, while intercalated and striated ducts maintained their size but occupied a greater relative volume in submandibular glands from irradiated compared to control animals. In addition, no inflammation or fibrosis was observed in the irradiated tissues. Carbachol- or thapsigargin-stimulated mobilization of Ca2+ was similar in dispersed submandibular gland cells from control and irradiated animals. Further, [Ca2+]i imaging of individual ducts and acini from control and irradiated groups showed, for the first time, that mobilization of Ca2+ in either cell type was not altered by the radiation treatment. The carbachol-stimulated, bumetanide-sensitive component of the Na+/K+/ 2Cl- cotransport activity was also similar in submandibular gland cells from control and irradiated animals. These data demonstrate that a single dose of gamma radiation induces a progressive loss of submandibular gland tissue and function. This loss of salivary flow is not due to chronic inflammation or fibrosis of the gland or an alteration in the neurotransmitter signaling mechanism in the acinar or ductal cells. The radiation-induced decrease in fluid secretion appears to be related to a change in either the water-handling capacity of the acini or the number of acinar cells in the gland.

Animals↗

PubMed1996

Role of nitric oxide in induction of inflammatory fluid secretion by the mucosa of the feline gallbladder.

BACKGROUND & AIMS: Nitric oxide is synthesized from L-arginine and is metabolized to nitrate and nitrite. This study evaluates the effects of a pharmacological blockade of NO synthesis on fluid transport by the inflamed gallbladder mucosa. METHODS: Experiments were performed in cats with cholecystitis and in control animals. NO synthase activity was measured in gallbladder tissue; the enzyme was characterized by immunoblotting techniques and localized by immunofluorescence. Fluid transport and release of nitrate and nitrite by the gallbladder mucosa and bile and bile salt secretion from the liver were registered simultaneously in vivo. RESULTS: Fluid secretion in inflamed gallbladders was reversed to a net absorption in response to the NO synthase blockers N omega-nitro-L-arginine and aminoguanidine, and formation of nitrate was reduced. The effects were reversed by L-arginine. Increased levels of inducible NO synthase in inflamed gallbladders were shown by immunoblotting, by immunofluorescence (mainly in macrophages), and by Ca(2+)-independent [3H]citrulline formation from [3H]arginine. The NO synthase blockers had no effect on gallbladder fluid transport in normal gallbladders. CONCLUSIONS: Increased levels of inducible NO synthase activity are shown in inflamed gallbladders, and a pharmacological blockade of this enzyme blocks fluid secretion and decreases nitrate release from the mucosa.

Analysis of Variance↗

PubMed2001

Dynamics of protein and fluid secretion from the major salivary glands of rat: relevance of research findings to clinically observed defective secretion in cystic fibrosis.

Although there are indications of a defect in secretion of protein from exocrine cells in cystic fibrosis (CF), this remains an aspect of CF research that has not been adequately addressed. Using salivary glands of rat as model systems, and following the effects of parasympathetic and sympathetic autonomic nerve stimulation on these glands, we demonstrate the existence of three separate pathways through which secretion of protein can be evoked from serous and mucous exocrine cells. These pathways allow the secretion of proteins from the intracellular compartments in a constitutive, intermediate or regulated manner. The primary aspects of secretory profile including concentration and the degree of hydration of secreted material differ greatly between the pathways, are cell type specific, and presumably are a direct consequence of controlled changes in the levels of second messengers induced upon stimulation of these cells. As previously published reports suggest that only the beta-adrenergic regulated pathway is affected by CF, differences between the pathways in their secretory profiles may influence the development of lung disease, through disparate disturbances in the secretion of protein and fluid from serous and mucous cells of the submucosal glands that line the bronchiolar tree in humans. We gratefully acknowledge support from The Wellcome Trust and from The European Union Biomed II Programme.

Amylases↗

PubMed1984

Relationship between rete testis fluid secretion and testicular structure in the ram.

A rete testis cannulation technique was used to compare the secretion of rete testis fluid with the production of spermatozoa and histological testicular parameters in Ile-de-France rams. Thirteen testes were cannulated and rete testis fluid variables were compared to histological variables of the same testis. The rate of flow of rete testis fluid was significantly (P less than or equal to 0.05%) correlated with testicular size, the area of the walls of the seminiferous tubules and the volume of the Leydig cells. These two latter factors accounted for 66% of the variation in the flow of rete testis fluid.

Animals↗

PubMed1981

Seasonal variations in rete testis fluid secretion and sperm production in different breeds of ram.

Production of spermatozoa and secretion of rete testis fluid (RTF) in rams was assessed by a rete testis cannulating technique. Four breeds (Ile-de-France, Romanov, Préalpes du Sud and cross-breed Romanov) were studied throughout the year. Inhibitory effects of the cannulation process on spermatogenesis were observed for some animals. Between-breed differences were found in sperm concentration and flow rate of the RTF. The seasonal variations in the daily sperm production of the testis were more pronounced for Ile-de-France rams than for the other breeds. There was a seasonal variation in the flow rate of RTF in Ile-de-France rams, the minimum flow being in February (winter) and the maximum in August-September (autumn).

Animals↗

PubMed2003

CFTR pharmacology and its role in intestinal fluid secretion.

The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl(-) channel expressed in epithelial cells in the airways, pancreas, intestine and other fluid-transporting tissues. Cystic fibrosis is caused by mutations in the CFTR, resulting in impaired Cl(-) transport and plasma membrane targeting. CFTR is expressed in the lumenal membrane of enterocytes, where it functions as the principal pathway for secretion of Cl(-) and fluid in enterotoxin-induced secretory diarrheas such as cholera. Small-molecule CFTR inhibitors reduce enterotoxin-induced intestinal fluid secretion in animal models. CFTR inhibition might also reduce intestinal fluid losses in cholera and possibly in other infectious and non-infectious diarrheas.

Animals↗

PubMed1981

New approaches to regulation of fluid secretion in airways.

Physiologic, morphologic, biochemical, and immunologic methods have been used to study cholinergic and adrenergic regulation of airway submucosal gland secretion. Using a newly developed micropipette method, we can now measure the rate of fluid flow from each individual gland duct and we can harvest these secretions for specific chemical analysis. Stimulation of both the cholinergic and adrenergic systems affect gland secretions. The vagus nerves are the pathways for many reflexes affecting secretion: laryngeal, gastric and carotid body chemoreceptor stimulation accelerate the fluid production, and lung inflation (Hering-Breuer reflex) inhibits fluid secretion. Stimulation by cholinergic, muscarinic agonists depletes both mucous and serous cells, so vagal reflexes probably produce mixed secretions. In contrast, alpha-adrenergic agonists deplete serous cell contents, release high concentrations of lysozyme and produce large volumes of fluid with a low protein concentration, while beta-adrenergic stimulation may selectively deplete mucous cells, releases little lysozyme and produces scanty fluid with a high protein concentration. The significance of this cholinergic and adrenergic modulation on cough and ciliary clearance are important subjects for future study.

Animals↗

PubMedDate not supplied

The effect of transport-blocking drugs on secretion of fluid and electrolytes by the mandibular gland of red kangaroos, Macropus rufus.

Mechanisms of primary fluid formation by macropodine mandibular glands were investigated in anaesthetized red kangaroos using ion-transport and carbonic anhydrase inhibitors. Bumetanide at carotid plasma concentrations of 0.005-0.1 mmol/l progressively reduced a stable, acetylcholine-evoked flow rate of 1.02 +/- 0.024 ml/min to 0.16 +/- 0.016 ml/min (mean +/- SEM). Concurrently, saliva [Na], [Cl] and osmolality decreased, [K] and [HCO3] increased and HCO3 excretion was unaffected. High-rate cholinergic stimulation was unable to increase salivary flow above 12 +/- 1.5% of that for equivalent pre-bumetanide stimulation. Furosemide (1.0 mmol/l) and ethacrynate (0.5 mmol/l) caused depression of salivary flow and qualitatively similar effects on ion concentrations to those of bumetanide. Amiloride (up to 0.5 mmol/l) caused no reduction in salivary flow rates or [Na] but decreased [K] and [Cl] and increased [HCO3]. When compared with bumetanide alone, amiloride combined with bumetanide further augmented [K] and [HCO3] and lowered [Cl], but had no additional effects on Na or flow. At the higher level, 4-acetamido-4'- isothiocyanatostilbene-2,2'disulphonic acid (SITS) (0.05 and 0.5 mmol/l) stimulated fluid output, increased [HCO3] and [protein], and depressed [Na], [K] and [Cl]. Relative to bumetanide alone, SITS given with bumetanide had no additional effects on salivary flow or electrolytes. Methazolamide (0.5 mmol/l) in combination with bumetanide curtailed the decrease in [Cl] and the increases in [K] and [HCO3] associated with bumetanide. The residual methazolamide-resistant HCO3 excretion was sufficient to support 2-6% of primary fluid secretion. It was concluded that secretion of primary fluid by the kangaroo mandibular gland is initiated mainly (> 90%) by Cl transport resulting from Na-K-2Cl symport activity. A small proportion of the fluid secretion (up to 6%) appears to be supported by HCO3 secretion. No evidence was found for fluid secretion being dependent on Cl transport involving Na/H and Cl/HCO3 antiports or on HCO3 synthesis involving carbonic anhydrase.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

PubMed1993

Involvement of the myenteric plexus in the cholera toxin-induced net fluid secretion in the rat small intestine.

BACKGROUND: The enteric nervous system is responsible in vivo for most of the change in fluid transport induced by cholera toxin. The aim of the present study was to investigate the importance of the myenteric plexus in the Intramural reflex responsible for this secretion. METHODS: Long-term ablation of the myenteric plexus was achieved by serosal application of benzalkonium chloride on jejunal segments in rats. RESULTS: The treated segments without functioning myenteric plexus showed a normal net fluid absorption. Cholera toxin in this segment only induced a reduction of fluid absorption, whereas in a nontreated ileal segment it concomitantly induced a conspicuous net fluid secretion. Intravenous hexamethonium did not change the cholera toxin response in the treated jejunal segments, whereas vasoactive intestinal polypeptide elicited a marked secretion. CONCLUSIONS: Benzalkonium chloride treatment eliminated the ability of cholera toxin to induce intestinal secretion. Thus, all afferent fibers in the intramural secretory reflex activated by cholera toxin are probably conveyed via the myenteric plexus, which functions as the integrating center in the enteric nervous system. The Ussing chamber technique using stripped intestinal preparations cannot be used when studying effects of luminal secretagogues.

Animals↗

PubMed1999

Contributions of K+:Cl- cotransport and Na+/K+-ATPase to basolateral ion transport in malpighian tubules of Drosophila melanogaster.

Mechanisms of Na+ and K+ transport across the basolateral membrane of isolated Malpighian tubules of Drosophila melanogaster were studied by examining the effects of ion substitution and putative inhibitors of specific ion transporters on fluid secretion rates, basolateral membrane potential and secreted fluid cation composition. Inhibition of fluid secretion by [(dihydroindenyl)oxy]alkanoic acid (DIOA) and bumetanide (10(-)4 mol l-1) suggested that a K+:Cl- cotransporter is the main route for K+ entry into the principal cells of the tubules. Differences in the effects of bumetanide on fluxes of K+ and Na+ are inconsistent with effects upon a basolateral Na+:K+:2Cl- cotransporter. Large differences in electrical potential across apical (>100 mV, lumen positive) and basolateral (<60 mV, cell negative) cell membranes suggest that a favourable electrochemical gradient for Cl- entry into the cell may be used to drive K+ into the cell against its electrochemical gradient, via a DIOA-sensitive K+:Cl- cotransporter. A Na+/K+-ATPase was also present in the basolateral membrane of the Malpighian tubules. Addition of 10(-)5 to 10(-)3 mol l-1 ouabain to unstimulated tubules depolarized the basolateral potential, increased the Na+ concentration of the secreted fluid by 50-73 % and increased the fluid secretion rate by 10-19 %, consistent with an increased availability of intracellular Na+. We suggest that an apical vacuolar-type H+-ATPase and a basolateral Na+/K+-ATPase are both stimulated by cyclic AMP. In cyclic-AMP-stimulated tubules, K+ entry is stimulated by the increase in the apical membrane potential, which drives K+:Cl- cotransport at a faster rate, and by the stimulation of the Na+/K+-ATPase. Fluid secretion by cyclic-AMP-stimulated tubules was reduced by 26 % in the presence of ouabain, suggesting that the Na+/K+-ATPase plays a minor role in K+ entry into the tubule cells. Malpighian tubules secreted a Na+-rich (150 mmol l-1) fluid at high rates when bathed in K+-free amino-acid-replete saline (AARS). Secretion in K+-free AARS was inhibited by amiloride and bafilomycin A1, but not by bumetanide or hydrochlorothiazide, which inhibit Na+:Cl- cotransport. There was no evidence for a Na+ conductance in the basolateral membrane of unstimulated or cyclic-AMP-stimulated tubules. Possible mechanisms of Na+ entry into the tubule cells include cotransport with organic solutes such as amino acids and glucose.

Animals↗