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PubMed1979

Fluid movements across rabbit ileum coupled to passive paracellular ion movements.

1. Theophylline (10 mM) and choleragen (1 x 10(-6) g ml.-1) abolish net fluid absorption by everted sacs of rabbit ileum. Triaminopyrimidine (20 mM) and ethacrynate (0.1 mM) prevent this inhibition of net fluid movement. Replacing Ringer Cl- with isethionate prevents the theophylline-dependent decrease in fluid absorption also. 2. Ouabain (0.1 mM) abolishes net fluid movements in both control and theophylline-treated tissue. 3. With ouabain present, hypertonic NaCl (200 mM) in the mucosal solution causes net fluid secretion (serosal-mucosal flux). With theophylline added to both the mucosal and serosal solution, net fluid absorption (mucosal-serosal flux) is observed (P less than 0.001). Triaminopyrimidine (20 mM), or ethacrynate (0.1 mM), or replacement of Ringer Na+ with choline, or Ringer Cl- with isethionate all prevent the theophylline-induced reversal of osmotic flow. 4. Theophylline increases passive net flux of Na+ and Cl- from mucosal solution containing hypertonic (200 mM) NaCl+ ouabain (0.1 mM) across sheets of ileum into serosal solution containing mannitol Ringer + ouabain. The increased passive Na+ flux is blocked by triaminopyrimidine and the increased Na+ and Cl- fluxes are blocked by ethacrynate (0.1 mM). 5. The suggested route of increased NaCl leakage is via the paracellular pathway as it is inhibited by triaminopyrimidine. The increase, itself, is a consequence of the increased passive permeability of the mucosal border to Cl-, induced by theophylline or choleragen. Water is apparently electro-osmotically coupled to the paracellular Na+ leakage (100 mole water mole-1 Na+), hence increased passive leakage reverses osmotic flow. In active tissue the lateral intercellular space contains hypertonic NaCl, and hence increased leakage of NaCl across the tight-junction in theophylline or choleragen-treated tissue gives rise to net fluid secretion.

Animals↗
PubMed1990

Oxygen consumption for K+ uptake during post-stimulatory activation of Na+, K(+)-ATPase in perfused rat mandibular gland.

1. In order to determine the stoichiometry of K+ uptake and ATP consumption by Na+, K(+)-ATPase in the isolated, perfused mandibular gland of the rat, oxygen consumption and net K+ uptake from the vascular side were measured during the recovery period following K+ depletion by stimulation with acetylcholine in combination with ouabain. 2. Acetylcholine (10(-6) M) induced fluid secretion and an initial, transient release of K+ from the gland. Addition of ouabain suppressed salivary fluid secretion and caused an additional, dose-dependent, transient release of K+. 3. With acetylcholine (10(-6) M), the oxygen consumption of the gland increased to 62.4 +/- 4.2 microliters/(g min) from a resting value of 12.9 +/- 1.2 microliters/(g min). The increased oxygen consumption was suppressed by ouabain, in a dose-dependent fashion. 4. Withdrawal of acetylcholine and ouabain induced a net uptake of K+ and, simultaneously, an increase in oxygen consumption. The cumulative K+ uptake and the increment of oxygen consumption during the recovery period were dependent on the concentration of used ouabain. 5. The rates of K+ uptake and ATP hydrolysis were compared during recovery, assuming that six moles of ATP were hydrolysed for each mole of oxygen consumed. The data obtained during the later phase of the recovery lay on a single straight line with a slope of 1.8 for each of the various concentrations of ouabain, suggesting that the relationship between K+ uptake and energy consumption was linear. 6. Assuming the K+:ATP stoichiometry of the Na+, K(+)-ATPase to be 2:1, K+ would appear to be transported with ca 90% efficiency by Na+, K(+)-ATPase in the rat mandibular gland. Using 1.8-2.0 as a K+/ATP stoichiometry, the rate of primary active K+ uptake and the corresponding passive K+ efflux during secretion were estimated to be 20-22 mumol/(g min) from the oxygen consumption and the net K+ flux. 7. The passive K+ efflux was estimated, from the initial rate of K+ release caused by addition of 10(-3) M-ouabain, to be 30 mumol/g min). The discrepancy between the estimated active K+ uptake and passive K+ release (8-10 mumol/(g min] could be attributed to a secondary active K+ uptake process such as Na(+)-K(+)-2Cl-symport.

Acetylcholine↗
PubMedDate not supplied

Hormonal evidence for the dissemination through the cerebrospinal fluid, of secreting cells from invasive pituitary adenomas.

In 13 patients with invasive pituitary adenomas submitted to pituitary surgery (5 HGH-secreting adenomas, 6 prolactin-secreting adenomas, 2 non-secreting adenomas), the concentrations of HGH and prolactin (PRL) constantly decreased after operation both in the cerebrospinal fluid (CSF) and serum, and the CSF/serum ratio remained under one, with few exceptions. These last cases (2 with acromegaly, 2 with invasive prolactinomas), showed an increase of HGH or PRL concentrations in CSF when serum levels decreased; the CSF/serum ratio rose above one within 2 weeks post surgery in 2 patients, and within 2 years post surgery in another two. The circulation of CSF was not obstructed. This indicated the appearance of a new, extrapituitary source for secreting HGH or PRL directly into the CSF, a source which most probably developed through the dissemination, via CSF, of secreting cells from malignant pituitary adenomas.

Acromegaly↗
PubMed1988

A comparative study of the effects of four choline esters on the secretion of fluid and glycoprotein from rat submandibular glands.

The actions of four choline esters, acetylcholine (ACH), methacholine (MET), carbachol (CAR) and bethanechol (BET), on the secretion of saliva and the specific glycoprotein (GP) contained in the secretory cells of the submandibular gland (SMG) of the rat were compared under conditions with and without physostigmine (PHY). The ED50 values with respect to salivation were 17 mg/kg for ACH, 1060 micrograms/kg for BET, 810 micrograms/kg for MET and 75 micrograms/kg for CAR, whereas after pretreatment with PHY, ED50 values were lowered to 7.5 mg/kg for ACH and 212 micrograms/kg for MET, but remained unchanged for CAR and BET. SDS-polyacrylamide gel electrophoresis demonstrated that the saliva from the SMG elicited by the four choline esters contained GP I (130 KDa) and GP IV (21.5 KDa), characteristic of the acinus, and a band of GP III (31 KDa), which originates from the granular tubules. The order of intensity of these bands was band I much greater than band III = band IV. Among these bands, band I increased in intensity in a dose-dependent manner. These results suggest that the four choline esters act mainly on the acinar cells, but exert some effects on the granular tubules of the rat SMG.

Acetylcholine↗
PubMed1988

Structural and functional studies of the effects of sympathetic nerve stimulation on rabbit submandibular salivary glands.

Continuous sympathetic stimulation at 8-10 Hz caused intense vasoconstriction in the gland, so stimulation was generally given in an interrupted pattern to minimize this detrimental effect on secretion. Only a small increase in fluid secretion occurred; it became thick and tended to block the cannula; therefore in later experiments the main duct was not cannulated. After sympathetic stimulation there was substantial degranulation of acinar cells. However, as this was accompanied by little movement of water, the secreted mucosubstance distended the ductal lumina. The granular tubule cells were unchanged by sympathetic stimulation. Use of selective blocking agents revealed that the sympathetically-evoked secretion of acinar mucin was mediated mainly via beta-adrenoreceptor activation. As stimulation of the sympathetic nerves alone caused little additional formation of fluid, the effects of superimposing continuous low frequency sympathetic stimulation onto a background of low parasympathetic secretion were compared with similar parasympathetic stimulation alone of the contralateral gland. These double nerve stimulations did not augment the volume of fluid secreted, or cause morphological changes additional to those from parasympathetic stimulation alone. Nevertheless, it is likely that, under natural reflex conditions, sympathetic impulses can increase the amount of acinar mucosubstance secreted.

Animals↗
PubMed1980

Role of calcium in exocrine pancreatic secreation. VI. Characteristics of the paracellular pathway for divalent cations.

(1) The transepithelial permeability for Ca2+ and Mg2+ in the isolated rabbit pancreas has been studied. (2) Values for the permeability of the unstimulated pancreas were obtained either by adding radioactive tracers to the bathing medium and measuring their concentration in the secreted fluid under steady-state conditions, or by analysis of the Ca2+ and Mg2+ concentrations in the secreted fluid after correction for protein-bound divalent cations. (3) Both methods give almost the same results: 27 and 26% for Ca2+ and 21 and 18% for Mg2+, respectively; both values being expressed as the percentage of the concentrations in the bathing medium. (4) The amounts of Ca2+ and Mg2+, appearing in the secretory fluid after correction for protein-bound cations, are linearly related to the extracellular Ca2+ and Mg2+ concentrations in the bathing medium, which indicates passive permeation. The two cations appear to pass through the paracellular route in their hydrated form. (5) Stimulation with carbachol or pancreozymin causes an increase in the paracellular permeability. This increase is approximately equal for the two divalent cations. Its time dependence and magnitude depend on the concentration of the stimulant rather than on the type of stimulant.

Animals↗
PubMed1984

Effects of acidosis and carbonic anhydrase inhibition in the elasmobranch rectal gland.

We studied the effects of acidosis and carbonic anhydrase inhibition on rectal gland fluid secretion. In the anesthetized dogfish shark, Squalus acanthias, volume expanded by a constant infusion of Ringer solution, fluid formation was halved by severe systemic metabolic and respiratory acidosis (pH approximately 7.10) and carbonic anhydrase inhibition. Mild respiratory acidosis (pH approximately 7.6) equivalent to the measured systemic pH during carbonic anhydrase inhibition was without effect. Inhibition of rectal gland enzyme produced severe glandular acidosis, which is indicated by an increase in gland fluid PCO2 (from 7 to 26 mmHg) and HCO3- (from 1.2 to 2.4 mM) and a decrease in pH (from 6.7 to 6.4). Gland tissue total CO2 dropped from 18 to 11 mmol/kg. These changes occurred despite nearly 50% reduction in fluid formation, O2 consumption, and CO2 output. We propose that carbonic anhydrase facilitates CO2 transfer from sites of metabolism to capillary blood by its conversion to HCO3-. This maintains a tolerable intracellular acid-base milieu during stimulated fluid secretion.

Acidosis↗
PubMed1991

5-Hydroxytryptamine: a second diuretic hormone in Rhodnius prolixus.

Bioassays of 5-hydroxytryptamine (5-HT) in fifth-instar Rhodnius prolixus haemolymph using Calliphora salivary glands indicate that: (1) biologically active 5-HT is present, (2) in unfed animals there is not enough 5-HT to stimulate Malpighian tubule fluid secretion, and (3) there is enough 5-HT soon after the initiation of feeding to stimulate rapid tubule secretion. The 5-HT receptor antagonists ketanserin and spiperone reversibly and selectively inhibit 5-HT-induced fluid secretion, indicating the presence of specific 5-HT receptors on Rhodnius Malpighian tubules. The data provide evidence that 5-HT is a naturally occurring hormone acting with a previously described peptide hormone to regulate diuresis in this species.

Animals↗
PubMed1999

Vasoactive intestinal polypeptide is a potent regulator of bile secretion from rat cholangiocytes.

BACKGROUND & AIMS: Vasoactive intestinal polypeptide (VIP) is a neuropeptide with diverse biological functions including stimulatory effects on bile secretion. The effects of VIP on bile secretion and its site of action were examined. METHODS: Choleretic effects of VIP were examined using isolated perfused livers, hepatocyte couplets, isolated bile duct units, and cholangiocytes from rat liver. RESULTS: VIP (100 nmol/L) produced a small increase in bile flow and bile salt output in taurocholate-supplemented isolated perfused livers but had no significant effect on bile flow in the absence of bile salt supplements or on fluid secretion in isolated hepatocyte couplets. In addition, VIP significantly increased bile pH, bicarbonate concentration, and output in the isolated perfused livers from both normal and 2 week bile duct-ligated rats, although bile flow increased only in the bile duct-ligated model. VIP also produced a dose-dependent increase in fluid secretion in isolated bile duct units, which was inhibited significantly by VIP antagonist, a specific VIP receptor inhibitor. This VIP-stimulated secretory response in isolated bile duct units was more potent than those produced by bombesin or secretin. Neither somatostatin nor substance P inhibited the VIP response in isolated bile duct units. In contrast to secretin, VIP had no significant effect on adenosine 3', 5'-cyclic monophosphate (cAMP) levels in isolated cholangiocytes. CONCLUSIONS: VIP is a potent stimulant of fluid and bicarbonate secretion from cholangiocytes via cAMP-independent pathways, suggesting that this neuropeptide plays a major regulatory role in biliary transport and secretion.

Amino Acid Sequence↗
PubMed2002

Absence of tight junction formation in an allogeneic graft cell line used for developing an engineered artificial salivary gland.

An essential structural feature of fluid-secreting epithelial tissues is the presence of tight junctions. To develop a tissue-engineered organ capable of fluid secretion, the cellular component must establish these structures. As part of efforts to create an engineered artificial salivary gland, we have examined the ability of a candidate allogeneic graft cell line, HSG, to produce several key tight junction proteins, as well as to exhibit functional activities consistent with effective tight junction strand formation. In contrast to results obtained with a control kidney cell line, MDCK-II, HSG cells were unable to synthesize four important tight junction-associated proteins: ZO-1, occludin, claudin-1, and claudin-2. In addition, unlike MDCK-II cells, HSG cell monolayers could not restrict paracellular permeability. HSG cells were, thus, unable to generate significant transepithelial electrical resistance or serve as an effective barrier to osmotically imposed fluid movement. Furthermore, these two functional activities could not be reconstituted via the stable transfection of HSG cells with cDNAs encoding either claudin-1 or claudin-2. We conclude that because of their inability to form tight junctions, HSG cells are unsuitable for use as an allogeneic graft cell in an artificial salivary fluid secretory device. These studies also emphasize the importance of graft cell selection in artificial organ development, as certain required characteristics may be difficult to reengineer.

Cell Line↗
PubMed2002

Two nitridergic peptides are encoded by the gene capability in Drosophila melanogaster.

A Drosophila gene (capability, capa) at 99D on chromosome 3R potentially encodes three neuropeptides: GANMGLYAFPRV-amide (capa-1), ASGLVAFPRV-amide (capa-2), and TGPSASSGLWGPRL-amide (capa-3). Capa-1 and capa-2 are related to the lepidopteran hormone cardioacceleratory peptide 2b, while capa-3 is a novel member of the pheromone biosynthesis-activating neuropeptide/diapause hormone/pyrokinin family. By immunocytochemistry, we identified four pairs of neuroendocrine cells likely to release the capa peptides into the hemolymph: one pair in the subesophageal ganglion and the other three in the abdominal neuromeres. In the Malpighian (renal) tubule, capa-1 and capa-2 increase fluid secretion rates, stimulate nitric oxide production, and elevate intracellular Ca(2+) and cGMP in principal cells. Capa-stimulated fluid secretion, but not intracellular Ca(2+) concentration rise, is inhibited by the guanylate cyclase inhibitor methylene blue. The actions of capa-1 and capa-2 are not synergistic, implying that both act on the same pathways in tubules. The capa gene is thus the first to be shown to encode neuropeptides that act on renal fluid production through nitric oxide.

Amino Acid Sequence↗
PubMed1995

Fluid and protein secretion from ferret submandibular and parotid glands in response to sympathetic nerve stimulation or administration of sympathomimetics.

Electrical stimulation of the sympathetic innervation evoked secretion of submandibular and parotid saliva. By changing the mode of stimulation from a continuous to an intermittent one the fluid response increased and glandular blood flow improved. The volumes from the submandibular glands were larger than those from the parotid glands and further, the protein concentration of submandibular saliva was higher than that of parotid saliva. Adrenaline, isoprenaline and phenylephrine evoked larger fluid responses from submandibular than from parotid glands. However, the fluid response was small compared to the parasympathetic one. Substance P-evoked saliva was used as carrier for protein released by sympathetic nerve stimulation or administration of adrenaline and isoprenaline. In vitro tissues of submandibular and parotid glands responded to adrenaline with a dose-dependent release of protein. Taken together, the analytical pharmacology performed in vivo and in vitro, and including the antagonists phentolamine, dihydroergotamine, propranolol and metoprolol, showed that in submandibular glands, alpha(alpha 1)adrenoceptors were predominantly involved in fluid secretion and beta(beta 1)-adrenoceptors predominantly involved in protein secretion. In parotid glands, fluid secretion seemed solely to depend on alpha(alpha 1)-adrenoceptors, while beta(beta 1)-adrenoceptors seemed almost solely involved in protein secretion.

Animals↗
PubMed1971

Acute undifferentiated human diarrhea in the tropics. II. Alterations in intestinal fluid and electrolyte movements.

The nature and magnitude of fluid and electrolyte loss into the small intestine were defined by the marker perfusion technique in patients with acute undifferentiated diarrhea (AUD) in the tropics. The patients were divided into two groups according to their small bowel bacteriologic findings, namely those with a predominant Escherichia coli flora and those with a mixed flora. 11 normal subjects served as controls. Net jejunal fluid secretion occurred into the lumen in four of seven patients with E. coli flora and three of seven with a mixed flora. The magnitude of secretion in the jejunum was greater in the E. coli flora patients than in those with a mixed flora. Four E. coli patients and one mixed flora patient had net fluid secretion in the ileum, although the magnitude of secretion in this area was less than in the jejunum. Intestinal fluid had higher bicarbonate concentration in the ileum than in the jejunum but was isotonic in both regions. It resembled in composition fluid from the same region of intestine in normal individuals. Recovery of normal fluid and electrolyte absorptive function was usually complete in both jejunum and ileum by 6-8 days after onset of the disease. Increase in unidirectional flux rates for H(3)O and (24)Na occurred in acute E. coli flora diarrhea and returned to normal levels in recovery: increase in J(beta) (plasma to lumen flux) primarily accounted for the increase in fluid loss. Intestinal biopsy revealed no alterations in villous architecture.A relationship between small bowel fluid production and the presence of toxigenic strains of E. coli within the small bowel has been found for E. coli flora patients. In many respects this disease resembles acute cholera. The mixed flora group represents a less defined entity which requires further study.

Adolescent↗
PubMed1988

Discrepancy between effects of cholera toxin on net fluid movement and cAMP levels in rat jejunum, ileum, and colon.

Regional differences in the response to cholera toxin were evaluated in rat jejunum, ileum, and colon in vivo. Ligated intestinal loops were exposed to a supramaximal concentration of cholera toxin for 5 hr, and net fluid transport, adenosine 3',5'-monophosphate (cAMP) concentrations, and adenylate cyclase and phosphodiesterase activities of mucosal homogenates were determined. The fluid transport response and the specific activities of adenylate cyclase (with and without cholera toxin) and phosphodiesterase declined progressively from the jejunum to the colon. In contrast, cAMP concentrations (with and without cholera toxin) were lowest in the jejunum and highest in the colon. These results demonstrate that cAMP concentrations of the total mucosal homogenate do not parallel cholera toxin-induced fluid secretion in the three intestinal segments. Rather, the activities of adenylate cyclase and phosphodiesterase suggest a relation between fluid secretion and the turnover of cAMP.

Adenylyl Cyclases↗
PubMed2004

cAMP potentiates ATP-evoked calcium signaling in human parotid acinar cells.

In salivary acinar cells, intracellular calcium ([Ca(2+)](i)) signaling plays an important role in eliciting fluid secretion through the activation of Ca(2+)-activated ionic conductances. Ca(2+) and cAMP have synergistic effects on fluid secretion such that peak secretion is elicited following activation of both parasympathetic and sympathetic pathways. We have recently demonstrated that cAMP exerts effects on Ca(2+) release, through protein kinase A (PKA)-mediated phosphorylation of inositol 1,4,5-trisphosphate receptors (InsP(3)R) in mouse parotid acinar cells. To extend these findings, in the present study cross-talk between Ca(2+) signaling and cAMP pathways in human parotid acinar cells was investigated. In human parotid acinar cells, carbachol stimulation evoked increases in the [Ca(2+)](i) and the initial peak amplitude was enhanced following PKA activation, consistent with reports from mouse parotid. Stimulation with ATP also evoked an increase in [Ca(2+)](i). The ATP-evoked Ca(2+) elevation was largely dependent on extracellular Ca(2+), suggesting the involvement of the P2X family of purinergic receptors. Pharmacological elevation of cAMP resulted in a approximately 5-fold increase in the peak [Ca(2+)](i) change evoked by ATP stimulation. This enhanced [Ca(2+)](i) increase was not dependent on intracellular release from InsP(3)R or ryanodine receptors, suggesting a direct effect on P2XR. Reverse transcription-polymerase chain reaction and Western blot analysis confirmed the presence of P2X(4)R and P2X(7)R mRNA and protein in human parotid acinar cells. ATP-activated cation currents were studied using whole cell patch clamp techniques in HEK-293 cells, a null background for P2XR. Raising cAMP resulted in a approximately 4.5-fold enhancement of ATP-activated current in HEK-293 cells transfected with P2X(4)R DNA but had no effects on currents in cells expressing P2X(7)R. These data indicate that in human parotid acinar cells, in addition to modulation of Ca(2+) release, Ca(2+) influx through P2X(4)R may constitute a further locus for the synergistic effects of Ca(2+) and PKA activation.

Adenosine Triphosphate↗