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PubMed1999

Modulation of carbachol-induced Cl(-) currents and fluid secretion by isoproterenol in rat submandibular acinar cells.

The effects of muscarinic and beta-adrenergic agonists on Cl(-) currents in acinar cells were investigated to clarify their role in the regulation of fluid secretion in rat perfused submandibular glands. Additions of isoproterenol (IPR) at 10(-8) to 10(-6) M and 8-(4-chlorophenylthio)-cyclic AMP (CPT-cAMP) at 10(-3) M to the perfusate suppressed carbachol (CCh; 10(-6) M)-induced fluid secretion. IPR and CPT-cAMP also diminished CCh-induced oscillatory Cl(-) current and increased CCh-stimulated non-oscillatory Cl(-) current. Propranolol blocked the effect of IPR on fluid secretion. IPR did not modulate the CCh-induced increase in intracellular concentration of calcium ions and intracellular pH in isolated cells. Propranolol blocked IPR-induced changes in Cl(- )currents, while propranolol itself increased CCh-induced K(+) current and reduced CCh-induced oscillatory Cl(-) current. Increasing external osmolarity with 50 mM sucrose abolished IPR-enhanced non-oscillatory Cl(-) current. Neither CCh-induced oscillatory Cl(-) current nor IPR-induced suppression of the oscillatory Cl(-) current was influenced by the hypertonicity. Perfusion of the gland with the hypertonic solution did not affect the IPR-induced suppression of fluid secretion. These results suggest that IPR induces the suppression of CCh-induced oscillatory Cl(-) current and potentiation of the non-oscillatory Cl(-) current via an increase in cyclic AMP level, and that suppression of the oscillatory Cl(-) current by IPR may contribute to the inhibition of fluid secretion from submandibular glands.

Adrenergic beta-Agonists↗
PubMed1985

Pancreatic fluid secretion and protein hyperconcentration in cystic fibrosis.

To study pancreatic protein and water secretion in 28 patients with cystic fibrosis and 21 controls matched for pancreatic acinar function as defined by trypsin secretion, we used a quantitative-marker perfusion technique and continuous intravenous secretin-pancreozymin stimulation. Regardless of the level of pancreatic acinar function, secretions from the patients contained significantly higher concentrations of protein than those from the controls. Total protein output and albumin:protein ratios were not increased in secretions from the patients, but their fluid secretion was significantly decreased at any level of pancreatic function. A significant linear correlation was found between protein and volume secretion in the patients (r = 0.86, P less than 0.001), most of whom had a fluid output of less than 4.2 ml per kilogram of body weight per hour. No such relation was found in the control subjects, whose flow was always above 4.2 ml per kilogram per hour. We conclude that fluid secretion in patients with cystic fibrosis may be a rate-limiting factor in protein output and that a limited flow of hyperconcentrated protein secretions may predispose to protein precipitation and ductal obstruction in the pancreas.

Adolescent↗
PubMed2006

The role of aquaporin water channels in fluid secretion by the exocrine pancreas.

The mammalian exocrine pancreas secretes a near-isosmotic fluid over a wide osmolarity range. The role of aquaporin (AQP) water channels in this process is now becoming clearer. AQP8 water channels, which were initially cloned from rat pancreas, are expressed at the apical membrane of pancreatic acinar cells and contribute to their osmotic permeability. However, the acinar cells secrete relatively little fluid and there is no obvious defect in pancreatic function in AQP8 knockout mice. Most of the fluid secreted by the pancreas is generated by ductal epithelial cells, which comprise only a small fraction of the gland mass. In the human pancreas, secretion occurs mainly in the intercalated ducts, where the epithelial cells express abundant AQP1 and AQP5 at the apical membrane and AQP1 alone at the basolateral membrane. In the rat and mouse, fluid secretion occurs mainly in the interlobular ducts where AQP1 and AQP5 are again co-localized at the apical membrane but appear to be expressed at relatively low levels. Nonetheless, the transepithelial osmotic permeability of rat interlobular ducts is sufficient to support near-isosmotic fluid secretion at observed rates. Furthermore, apical, but not basolateral, application of Hg(2+) significantly reduces the transepithelial osmotic permeability, suggesting that apical AQP1 and AQP5 may contribute significantly to fluid secretion. The apparently normal fluid output of the pancreas in AQP1 knockout mice may reflect the presence of AQP5 at the apical membrane.

Animals↗
PubMed1984

The mechanism of fluid secretion in the rabbit pancreas studied by means of various inhibitors.

In order to increase our understanding of the mechanism of pancreatic fluid secretion we have studied the effects of various transport inhibitors on this process in the isolated rabbit pancreas. In this preparation, a high rate of unstimulated fluid secretion occurs, which probably originates from the ductular cells. Inhibitory are ouabain, furosemide, bumetanide, piretanide, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) and acetazolamide, with their half-inhibitory concentrations: 2 X 10(-6) M (ouabain), 1.3 X 10(-3) M (furosemide), 2.2 X 10(-3) M (bumetanide and piretanide) and 1.4 X 10(-4) M (SITS). With acetazolamide a maximal inhibition of only 20% is found at 10(-3) M. Amiloride (10(-3) M) has no effect on pancreatic fluid secretion. The inhibitory effects on HCO-3 output are always larger and those on Cl- output lower than those on fluid secretion. The results suggest that the ouabain-sensitive (Na+ + K+)-ATPase system provides the energy for a Na+-gradient-driven Cl--HCO-3-exchange transport system, sensitive to the loop diuretics furosemide, bumetanide and piretanide and to SITS. This system would drive the transcellular transport of HCO-3 and secondarily that of cations, Cl- and water.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed2006

Acinar origin of CFTR-dependent airway submucosal gland fluid secretion.

Cystic fibrosis (CF) airway disease arises from defective innate defenses, especially defective mucus clearance of microorganisms. Airway submucosal glands secrete most airway mucus, and CF airway glands do not secrete in response to VIP or forskolin. CFTR, the protein that is defective in CF, is expressed in glands, but immunocytochemistry finds the highest expression of CFTR in either the ciliated ducts or in the acini, depending on the antibodies used. CFTR is absolutely required for forskolin-mediated gland secretion; we used this finding to localize the origin of forskolin-stimulated, CFTR-dependent gland fluid secretion. We tested the hypothesis that secretion to forskolin might originate from the gland duct rather than or in addition to the acini. We ligated gland ducts at various points, stimulated the glands with forskolin, and monitored the regions of the glands that swelled. The results supported an acinar rather than ductal origin of secretion. We tracked particles in the mucus using Nomarski time-lapse imaging; particles originated in the acini and traveled toward the duct orifice. Estimated bulk flow accelerated in the acini and mucus tubules, consistent with fluid secretion in those regions, but was constant in the unbranched duct, consistent with a lack of fluid secretion or absorption by the ductal epithelium. We conclude that CFTR-dependent gland fluid secretion originates in the serous acini. The failure to observe either secretion or absorption from the CFTR and epithelial Na(+) channel (ENaC)-rich ciliated ducts is unexplained, but may indicate that this epithelium alters the composition rather than the volume of gland mucus.

Animals↗
PubMed1979

Relationship between hormonal activation of phosphatidylinositol hydrolysis, fluid secretion and calcium flux in the blowfly salivary gland.

The addition of 5-hydroxytryptamine to the isolated blowfly salivary gland stimulates fluid secretion, transepithelial calcium transport and the breakdown of 32P- or 3H-labelled phosphatidylinositol The breakdown of [32P]phosphatidylcholine and [32P]-phosphatidylethanolamine was not stimulated by 5-hydroxytryptamine. In salivary glands incubated with myo-[2-3H]inositol for 1--3 h, more than 95% of the label retained by the tissue was in the form of phosphatidylinositol. The addition of 5-hydroxytryptamine resulted in an increase in the accumulation of label in intracellular inositol 1:2-cyclic phosphate, inositol 1-phosphate and free inositol along with an increase in the release of [3H]inositol to the medium and saliva. The release of [3H]inositol to the medium served as a sensitive indicator of phosphatidylinositol breakdown. The release of [3H]inositol was not increased by cyclic AMP or the bivalent-cation ionophore A23187 under conditions in which salivary secretion was accelerated. The stimulation of fluid secretion by low concentrations of 5-hydroxytryptamine was potentiated by 3-isobutyl-1-methylxanthine, which had no effect on inositol release. The stimulation of fluid secretion by 5-hydroxytryptamine was greatly reduced in calcium-free buffer, but the breakdown of phosphatidylinositol continued at the same rate in the absence of calcium. These results support the hypothesis that breakdown of phosphatidylinositol by 5-hydroxytryptamine is involved in the gating of calcium.

Animals↗
PubMed1990

Stimulatory effects of 5-hydroxytryptamine on fluid secretion and transmural potential difference in rat small intestine are mediated by different receptor subtypes.

The rise in transmural potential difference (PD) and the fluid secretion induced by 5-hydroxytryptamine (5-HT) were measured in rat small intestine in-vivo. Both cisapride and ketanserin abolished the 5-HT-induced rise in systolic blood pressure mediated by 5-HT2 receptors. Cisapride inhibited the 5-HT-induced increases in the transintestinal PD, but over the same dose range it had no effect on the fluid secretion induced by 5-HT. In contrast, ketanserin caused a dose-dependent reduction in 5-HT-induced fluid secretion at doses that failed to influence the rise in PD. It is concluded that different receptors are responsible for the effects of 5-HT on fluid secretion and electrical activity in the rat small intestine.

Animals↗
PubMed1993

Serotonin antagonists inhibit sennoside-induced fluid secretion and diarrhea.

The aim of this study was to investigate whether 5-hydroxytryptamine (serotonin, 5-HT) is involved in the mediation of sennoside-induced colonic fluid secretion and diarrhea. Oral administration of purified sennosides (25, 40 and 64 mg/kg) dose-dependently reversed net fluid absorption to net fluid secretion, enhanced the incidence of diarrhea and stimulated the release of 5-HT into the colonic lumen from 7.1 to 17.3 ng/g wet weight. The 5-HT2 antagonist ketanserin and the 5-HT3 antagonist tropisetron dose-dependently but only partially reduced sennoside (40 mg/kg)-induced fluid secretion whereas the 5-HT3 antagonist granisetron dose-dependently reduced and at 300 micrograms/kg totally abolished sennoside-induced secretion. Granisetron, but not ketanserin and tropisetron, reduced the incidence of diarrhea in sennoside-treated rats, indicating the involvement of 5-HT also in acceleration of large intestinal transit. It is concluded that 5-HT is an important mediator both of sennoside-induced fluid secretion in the rat colon and of diarrhea.

Animals↗
PubMed1989

Renal epithelial fluid secretion and cyst growth: the role of cyclic AMP.

Transepithelial fluid secretion has been postulated to account for the accumulation of fluid within hereditary and acquired renal cysts, but no such mechanism has been demonstrated in human kidney epithelium. It is shown here that transepithelial fluid secretion was stimulated by prostaglandin E1 (PGE1), forskolin, 8-Br-cyclic AMP, and 1-methyl-3-isobutylxanthine in polarized monolayers of established renal cell lines (MDCK and rat glomerular epithelial cells) and in monolayer cultures derived from the cyst walls of human autosomal dominant polycystic kidney disease and from epithelial cells of normal human renal cortex. Treatment with cyclic AMP agonists caused the same cells, when dispersed within a gel matrix of type I collagen (Vitrogen), to proliferate and form spherical fluid-filled monolayered cysts. Our findings suggest that increased intracellular cyclic AMP levels may have a critical role in the formation and expansion of hereditary and acquired renal cysts.

1-Methyl-3-isobutylxanthine↗
PubMed2004

Basolateral ion transport mechanisms during fluid secretion by Drosophila Malpighian tubules: Na+ recycling, Na+:K+:2Cl- cotransport and Cl- conductance.

Mechanisms of ion transport during primary urine formation by the Malpighian tubule of Drosophila melanogaster were analyzed through measurements of fluid secretion rate, transepithelial ion flux, basolateral membrane potential (V(bl)) and intracellular activities of K(+) (a(K)(i)) and Cl(-) (a(Cl)(i)). Calculation of the electrochemical potentials for both ions permitted assessment of the possible contributions of K(+) channels, Na(+):K(+):2Cl(-) cotransport, and K(+):Cl(-) cotransport, to net transepithelial ion secretion across the basolateral membrane. The data show that passive movement of both K(+) and Cl(-) from cell to bath is favoured across the basolateral membrane, indicating that both ions are actively transported into the cell. Contributions of basolateral K(+) channels or K(+):Cl(-) cotransporters to net transepithelial ion secretion can be ruled out. After prior exposure of tubules to ouabain, subsequent addition of bumetanide reduced fluid secretion rate, K(+) flux and Na(+) flux, indicating a role for a Na(+):K(+):2Cl(-) cotransporter in fluid secretion. Addition of the K(+) channel blocker Ba(2+) had no effect on a(K)(i) or a(Cl)(i). Addition of Ba(2+) unmasked a basolateral Cl(-) conductance and the hyperpolarization of V(bl) in response to Ba(2+) was Cl(-)-dependent. A new model for fluid secretion proposes that K(+) and Cl(-) cross the basolateral membrane through a Na(+)-driven Na(+):K(+):2Cl(-) cotransporter and that most of the Na(+) that enters the cells is returned to the bath through the Na(+)/K(+)-ATPase.

Animals↗
PubMed2005

The hormonal control of uterine luminal fluid secretion and absorption.

The secretion of uterine luminal fluid initially provides a transport and support medium for spermatozoa and unimplanted embryos, while the absorption of uterine luminal fluid in early pregnancy results in the closure of the lumen and allows blastocysts to establish intimate contact with the uterine epithelium. We have established an in vivo perfusion technique of the lumen to study the hormonal control of the events in the peri-implantation period. Fluorescein-labelled dextran was included in the perfusion medium to monitor fluid movements and the concentrations of Na(+) and CI(-) ions in the effluent were monitored. Using an established regimen of steroid treatment of ovariectomized rats mimicking early pregnancy, oestradiol caused fluid secretion, while progesterone resulted in an amiloride-sensitive fluid absorption. Fluid absorption peaked at about the expected time of implantation. The effect of progesterone could be inhibited by treatment with a high dose of oestradiol, by the anti-progestin RU486, and by the presence of an intra-uterine contraceptive device. Studies of expression of Na(+) and CI(-) channels (ENaC, CFTR) indicated that these channels were subject to tissue-specific regulation within the uterus, but more work is required to determine their role and the factors controlling their abundance and localization in early pregnancy.

Animals↗
PubMed1973

Pathogenesis of salmonellosis. Studies of fluid secretion, mucosal invasion, and morphologic reaction in the rabbit ileum.

Strains of Salmonella typhimurium were studied in the ligated rabbit ileal loop model to gain insight into the mechanisms whereby bacteria which invade the gastrointestinal mucosa evoke fluid exsorption. The organisms employed differed in various biologic attributes including the ability to invade the ileal epithelium, multiply within the mucosa, elicit an acute inflammatory reaction, and disseminate across the intestinal wall. Some strains provoked small intestinal fluid exsorption although these did not elaborate enterotoxin. Only those strains which invaded the mucosa were accompanied by either mucosal inflammation or fluid exsorption. Noninvasive strains produced neither histologic abnormalities nor fluid secretion. While strains which invaded the mucosa caused an acute inflammatory reaction, not all such strains evoked fluid secretion. Furthermore, there was no correlation in ability of invasive organisms to evoke fluid secretion or in the intensity of mucosal inflammation, number of intramucosal salmonellae, or in ability to disseminate from the rabbit ileum. These observations suggest that, as is the case in shigellosis, mucosal invasion may be a necessary factor for the intestinal fluid loss in salmonellosis. A bacterial property or factor, in addition to invasion of the gastrointestinal mucosa, seems to be responsible for fluid exsorptin. However, it is unlikely that a salmonella enterotoxin comparable to that elaborated by Vibrio cholerae, toxigenic Escherichia coli, or Shigella dysenteriae 1 is related to fluid secretion in salmonellosis.

Animals↗
PubMed1986

The net fluid secretion caused by cyclic 3'5'-guanosine monophosphate in the rat jejunum in vivo is mediated by a local nervous reflex.

The tissue concentration of cyclic 3'5'-guanosine monophosphate (cGMP) has been shown to increase in the small intestine when net fluid secretion is evoked by the heat-stable enterotoxine of Escherichia coli. Lipophilic cGMP analogues are also known to elicit intestinal fluid secretion. It is therefore believed that an increase in intracellular cGMP concentration in enterocytes mediates this secretion. The present study reports that the fluid secretion, elicited by placing two different cGMP analogues, dibutyryl-cGMP and 8-Br-cGMP, in the intestinal lumen of anaesthetized rats in vivo, is significantly inhibited by atropine, hexamethonium and lidocaine. It is proposed that cGMP activates a reflex in the enteric nervous system which, in part, explains the observed fluid secretion.

Acetylcholine↗
PubMed1989

Involvement of 5-hydroxytryptamine, prostaglandin E2, and cyclic adenosine monophosphate in cholera toxin-induced fluid secretion in the small intestine of the rat in vivo.

The diarrhea of cholera is considered to rely solely on a cyclic adenosine monophosphate-mediated secretory mechanism. However, both 5-hydroxytryptamine and prostaglandin E2 have been proposed to be involved in the pathogenesis of cholera. In vivo experiments were performed, therefore, in the rat jejunum to investigate the influence of purified cholera toxin on fluid secretion, luminal release of 5-hydroxytryptamine and prostaglandin E2, and formation of mucosal cyclic adenosine monophosphate. Also the effects of ketanserin, indomethacin, verapamil, and nifedipine on the named parameters were studied. Cholera toxin dose-dependently (0.1-0.5 microgram/ml) and time-dependently (1-5 h) increased mean net fluid secretion with a maximum response at 4 h. It also caused a significant (p less than 0.01) rise in release of 5-hydroxytryptamine and prostaglandin E2, in addition to formation of cyclic adenosine monophosphate. The dose-response curve for cholera toxin-induced fluid secretion was shifted to the right by indomethacin (10 mg/kg s.c.) and ketanserin (200 micrograms/kg s.c.), none of which caused a change in cholera toxin-induced release of 5-hydroxytryptamine. However, both agents significantly decreased the release of prostaglandin E2. Verapamil (0.2-9.5 micrograms/min i.a.) and nifedipine (0.05-0.5 microgram/min i.a.) dose-dependently reduced cholera toxin-induced fluid secretion. The estimated local concentrations at half-maximal inhibition were 5 x 10(-7) M verapamil and 5 x 10(-8) M nifedipine, respectively. The cholera toxin-induced increase in release of 5-hydroxytryptamine and prostaglandin E2 and formation of cyclic adenosine monophosphate was unaffected by verapamil. These results support the concept that cholera toxin-induced fluid secretion in vivo is caused, in part, by release of 5-hydroxytryptamine, which in turn stimulates formation of prostaglandin E2.

Animals↗
PubMed1997

Nitric oxide counteracts 5-hydroxytryptamine- and cholera toxin-induced fluid secretion and enhances the effect of oral rehydration solution.

The effects of pharmacological modulation of the nitric oxide (NO) pathway on intestinal fluid transport were studied in a model of ligated jejunal loops of anaesthetized rats in vivo. Close intraarterial infusion of 5-hydroxytryptamine (5-HT) (0.16 microg/min) induced net fluid secretion. Intravenous infusion of the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) (0.55 mg/kg per min) reversed net fluid absorption in controls to net secretion and significantly enhanced 5-HT-induced fluid secretion. 5-HT-induced net fluid secretion was inhibited by intravenous infusion of L-arginine (8.88 mg/kg per min), sodium nitroprusside (22.2 microg/kg per min), or 3-morpholino sydnonimine (SIN-1) (22.2 microg/kg per min). Intraluminal instillation of cholera toxin (0.5 microg/ml) induced net secretion, which was significantly enhanced by L-NAME and reduced by L-arginine. Another series of experiments was performed using a model of luminally perfused jejunal loops. Cholera toxin (10 microg/ml) induced profuse net fluid secretion also in this model. L-Arginine and sodium nitroprusside significantly enhanced net fluid absorption compared to controls and abolished the secretory effect of cholera toxin. Luminal perfusion with oral rehydration solution enhanced net absorption of fluid in controls and reversed cholera toxin-induced secretion to absorption. Intravenous infusion, but not intraluminal administration, of L-arginine significantly enhanced the antisecretory effect of oral rehydration solution. These results give further support to the existence of an intestinal NO-mediated proabsorptive tone, which also downregulates fluid secretion elicited by different enterotoxins or mediators of secretion. Intravenous administration of exogenous sources of NO counteracts intestinal fluid accumulation and augments the antisecretory effect of oral rehydration solution, findings which may lead to therapeutic consequences.

Animals↗
PubMed1997

Calcium channels and intestinal fluid secretion: an experimental study in vivo in rats.

Several mechanisms involved in nervous secretory reflex(es) of the enteric nervous system may be dependent on the flux of calcium across the plasma membrane, which may be controlled by voltage-gated calcium channels. In this study, we investigated the importance of plasma membrane calcium channels for intestinal fluid secretion. Two types of studies were performed, in which intestinal net fluid transport in anaesthetized rats was followed with a gravimetric method. First, the effects on intestinal fluid transport of placing A23187, a calcium ionophore, in the intestinal lumen was studied. A23187 induced in a dose-dependent manner a net fluid secretion, which was abolished by giving hexamethonium (10 mg kg(-1) body wt) i.v. or placing lidocaine (1% solution) on the intestinal serosa. Nifedipine (5.75 micromol kg(-1) body wt i.v.) also abolished the fluid secretion caused by the ionophore. In the second study, the effects of various calcium channel blockers (gadolinium chloride, nifedipine, verapamil) were tested on the cholera toxin-induced secretion. It was attenuated by luminal application of gadolinium chloride (1-10 mM) or nifedipine (10-200 microM). Intravenously administered nifedipine (2.5-5.75 micromol kg(-1) body wt) abolished cholera toxin-evoked secretion dose-dependently, whereas verapamil (0.05-1 micromol kg(-1) body wt) was without consistent effect. It is concluded that the fluid secretion evoked by placing A23187 in the intestinal lumen in vivo was induced via an activation of the enteric nervous system. Cholera secretion was attenuated or abolished by calcium channel blockers of the L- or N-type.

Anesthetics, Local↗
PubMed1979

Extracellular free calcium and fluid secretion by the rabbit lacrimal gland in vivo.

A possible role of extracellular free Ca2+ in methacholine-induced fluid secretion in the in vivo rabbit lacrimal gland has been investigated. Lowering the extracellular Ca2+ concentration by either intra-arterial injection or infusion of EGTA at doses which caused no systemic effects produced a dose related and reversible inhibition of methacholine-induced secretion. The inhibitory effect of EGTA was diminished when EGTA chelated with CaCl2 in varying concentration ratios was administered. On the other hand, intra-arterial injection of CaCl2 potentiated fluid secretion stimulated by submaximal doses of methacholine. These results suggest that fluid secretion from the rabbit lacrimal gland is dependent on the extracellular free Ca2+ concentration.

Animals↗
PubMed1989

TRH pharmacokinetics and nerve stimulation evoked prostatic fluid secretion during TRH infusion in the dog.

The pharmacokinetics of TRH have been determined in man and the rat as well as other species whose serum contains TRH degrading enzymes, TRH pharmacokinetics have not been determined in the dog. This species is unusual in that its serum contains little or no TRH degrading activity. TRH pharmacokinetics were determined from measurements of plasma TRH concentrations during and following a 1-h infusion of TRH, 20 micrograms.kg-1.min-1, into dogs bearing prostatic urethral cannula. During TRH administration prostatic fluid secretion was evoked by hypogastric nerve stimulation and the content of TRH immunoreactive material in prostatic fluid was determined. Prostatic fluid was also collected after hypogastric nerve stimulation in dogs that did not receive TRH infusion. The TRH plasma profile in TRH-infused dogs exhibited two-compartment characteristics with an initial half-time of 10.4 +/- 5.4 (mean +/- SD) min, a terminal half-time of 69.4 +/- 24 min, and a metabolic clearance rate of 7.64 +/- 4.48 ml.min-1.kg-1. These findings suggest that the half-time of TRH is longer, and its metabolic clearance rate is less, in the dog than in humans or rats. TRH administration was not associated with altered nerve induced prostatic fluid secretion. Prostatic fluid samples contained TRH immunoreactive material regardless of whether they were collected after epithelial cell stimulation with pilocarpine, or after hypogastric nerve stimulation. In contrast to previous results with vasoactive intestinal peptide, TRH does not acutely alter prostatic fluid secretion. As has been reported for prostatic tissue extracts, immunoreactive material is present in prostatic fluid and appears to arise from epithelial cells.

Animals↗