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PubMed1997

Prolactin increases ATP-dependent taurocholate transport in canalicular plasma membrane from rat liver.

The taurocholate (TC) maximal secretory rate (SRm) in the isolated perfused liver is increased in postpartum rats and ovariectomized rats treated with ovine prolactin (oPRL). The present studies were designed to characterize the mechanism(s) by which oPRL increases TC transport in the liver. oPRL (300 micrograms/day i.v. for 7 days) increased the SRm 1.6-fold from 185 to 364 nmol.min-1.mg protein-1 in the perfused rat liver and the maximal rate of transport for ATP-dependent transport 1.7-fold from 66 to 109 nmol.min-1.mg protein-1 in canalicular liver plasma membrane (cLPM) vesicles without changing the Michaelis constant (5-6 microM). The oPRL-mediated increases in biliary excretion in the perfused liver and ATP-dependent TC transport in cLPM vesicles were significantly inhibited by cycloheximide treatment (2 mg/kg). oPRL (300 micrograms/day iv for 7 days) increased expression of Ca(2+)-Mg(2+)-ecto-adenosinetriphosphatase mRNA sixfold and increased protein expression two- to threefold, but had no effect on the expression of P-glycoprotein (mdr1b and mdr2) mRNA. Thus the increase in ATP-dependent transport in cLPM vesicles due to oPRL treatment accounts for the increased TC SRm in the perfused liver. The oPRL-mediated increased TC transport may be associated with increased expression of proteins related to bile acid transport.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1985

Enzymatic activity of rat submandibular gland kallikrein released into blood.

Enzymatic activity of submandibular gland (SG) kallikrein released into saliva and blood was studied at rest and after autonomic nerve stimulation. Kallikrein was measured by an immunometric assay that allows measurement of immunoreactive kallikrein in complex with inhibitors as well as simultaneous determination of kallikrein enzymatic activity. Measurements using the chromogenic substrate S2266 gave identical results to the natural substrate kininogen. Endogenous SG kallikrein secretory rate was, at rest, 0.9 +/- 0.1 ng/min. Kallikrein secretion into blood in response to autonomic nerve stimulation paralleled that into saliva, and secretion was greatly enhanced by alpha-adrenergic stimulation. In plasma, kallikrein was bound to several inhibitors that completely or partially blocked the enzyme activity. In arterial and SG venous control plasma, 93 +/- 3 and 72 +/- 10% inhibition of kallikrein enzyme activity was observed, respectively. Sympathetic stimulation after administration of a beta-adrenergic blocker increased kallikrein enzyme activity 62 and 11 times in arterial and SG venous plasma, respectively, with a corresponding 78 +/- 8 and 70 +/- 8% inhibition of kallikrein enzyme activity. A fraction containing kallikrein resembling "free kallikrein" was always present in plasma.

Animals↗
PubMed1992

Corticoid regulation of atrial natriuretic factor secretion and gene expression.

This study investigated the acute effects of glucocorticoids and mineralocorticoids on atrial natriuretic factor (ANF) biosynthesis in vivo. Groups of male Sprague-Dawley rats were injected with 1 mg dexamethasone (Dex), 10 mg deoxycorticosterone acetate (DOCA) or vehicle alone. Different groups were studied after periods of 30 min to 8 h. Plasma and left atrial ANF concentrations and ANF mRNA levels were measured 2-8 h after corticoid injection. From 30 min to 2 h after injection, ANF mRNA was analyzed by quantitative and qualitative assessments. There was a two- to threefold increase in plasma levels of ANF in Dex-treated rats compared with controls at all time periods (P < 0.05). Although ANF plasma levels increased over time following DOCA treatment, they were not significantly different from control values. Dex treatment also increased normalized ANF mRNA levels 77% above control levels during the first 4 h after injection (P < 0.05). Thereafter there was a return of mRNA levels to that seen in controls. There was no qualitative difference in the ANF mRNA at any time as assessed by Northern hybridization. In contrast, DOCA increased ANF mRNA levels only after 8 h (P < 0.05). No significant changes in left atrial ANF content were noted during this study. In a separate study, Dex was administered to isolated left atria in vitro in a superfusion system. Superfusion with 2 x 10(-5) M Dex produced a 40% increase in ANF secretory rate within 20 min (P = 0.036). We conclude that Dex induces a direct rapid increase in ANF mRNA levels and ANF secretion in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Ba++ on the resting frog stomach: effects on electrical and secretory parameters.

Ba++ added to the nutrient solution bathing the resting frog stomach increased resistance, decreased the PD, and stimulated acid secretion. Under short-circuit conditions, the increase in H+-secretory rate was accompanied by a decrease in short-circuit current (I-sc). These changes were reversed by NaSCN (10 mM), suggesting that Ba++ had not impaired the current-generating mechanism per se. Histamine-induced acid secretion was associated with an increase in net Cl- flux, particularly in the N yields S flux (JNS). Ba++ increased acid secretion with no increase in JNS and a decrease in net Cl- flux. The effects of Ba++ were amplified by low-Cl- solutions. Histamine, in the presence of Ba++ and low-Cl- solutions, increased acid secretion and transmucosal resistance, suggesting the operation of a neutral pump in the secretion of HCl. It is concluded that Ba++ limits Cl- entry and also acts as a secretagogue.

Animals↗
PubMed1975

Plasma renin activity during ovine pregnancy.

Chronic intravascular catheterization in maternal, fetal, and neonatal sheep was utilized to assess basal plasma renin activity (PRA) and changes in PRA in response to furosemide. Maternal PRA increased from base-line levels during the last trimester of pregnancy and remained elevated for 12 wk postpartum. Fetal basal levels of PRA were variable but usually greater than maternal levels. Intravenous administration of furosemide to pregnant ewes resulted in a prompt and significant increase in maternal PRA with inconsistent changes in fetal PRA. Fetal and neonatal animals with low basal levels showed a significant increase in PRA; maternal PRA did not change. Animals with higher basal levels did not respond to the stimulus, perhaps reflecting a maximum renin secretory rate. These data are consistent with the conclusions that fetal renin originated predominantly from the fetal kidney, that fetal PRA receives no significant contribution from the maternal circulation, and that renin does not cross the ovine placenta.

Animals↗
PubMed1975

Potassium adaptation and Na-K-ATPase activity in mucosa of colon.

The specific activity of sodium-potassium-activated adenosine triphosphatase in the mucosa of the colon rises when the dietary load of potassium is increased. The change in enzymatic activity depends on the presence of intact adrenal glands, since adrenalectomy abolishes the response of Na-K-ATPase to potassium loading. The increased secretory rate of aldosterone normally evoked by potassium loading appears to mediate at least in part of the effect of potassium loading, since aldosterone induces a discernible increase in the specific activity of Na-K-ATPase in the colon of adrenalectomized rats.

Adenosine Triphosphatases↗
PubMed1976

Effects of salicylate and bile salt on ion transport by isolated gastric mucosa of the rabbit.

The effects of luminal addition of salicylate and taurocholate on ion transport by fundic mucosa were examined in vitro using isotopic and pH stat techniques. Salicylate, 3 mM, did not alter, but 20 mM caused a 40% decrease in, the acid secretory rate. Taurocholate, 20 mM, caused a transient, apparent cessation of acid secretion followed by stimulation. Salicylate, 3 or 20 mM, increased Na+ but not Cl- permeability at luminal pH 7. At luminal pH 4, however, salicylate increased Cl- in addition to Na+ and H+ permeability. Taurocholate, 10 or 20 mM, increased both cation and anion permeability at pH 7 and 4. Addition of salicylate or taurocholate results in stimulation of net Na+ transport. While salicylate and taurocholate increase cation permeability at pH 7, they have differing effects on acid secretion and anion permeability. The data suggest that salicylate and taurocholate alter cation permeability by different mechanisms and are consistent with the concept that enhanced diffusion of H+ into the tissue causes a nonspecific alteration in the permeability pathway.

Animals↗
PubMed1976

Inhibition of H+ secretion in the frog gastric mucosa by ATP and related compounds.

Addition of adenosine triphosphate (ATP) to the nutrient (submucosal-facing) solution of the histamine-stimulated in vitro frog (Rana pipiens) gastric mucosa produces a marked reduction in the H+ secretory rate and an increase in transmucosal potential difference (PD) and resistance in both Cl- and Cl-free media. The effects are reversible upon removal of ATP. The threshold concentration is between 1 and 2 mM, and 5 mM produce maximal inhibition. It is shown that the effects of ATP are not due to a change in pH or osmolarity of the nutrient fluid, or to a decrease in the Ca2+ and/or Mg2+ activities of the nutrient fluid. It is also shown that the inhibitory action of ATP is not dependent on a chelation complex between Ca2+ or Mg2+. Adenosine diphosphate also produces effects essentially the same as ATP whereas 5'-adenosine monophosphate and adenosine produce relatively little or no change.

Adenosine↗
PubMed2004

Secretion of lactoferrin and lysozyme by cultures of human airway epithelium.

Lactoferrin and lysozyme are important antimicrobial compounds of airway surface liquid, derived predominantly from serous cells of submucosal glands but also from surface epithelium. Here we compared release of these compounds from the following human cell cultures: primary cultures of tracheal epithelium (HTE), Calu-3 cells (a lung adenocarcinoma cell line frequently used as a model of serous gland cells), 16HBE14o- cells (an SV40 transformed line from airway surface epithelium), T84 cells (a colon carcinoma cell line), and human foreskin fibroblasts (HFF). For lysozyme, baseline secretory rates were in the order Calu-3 > 16HBE14o- > HTE T84 > HFF = 0; for lactoferrin, the only cell type showing measurable release was HTE; for mucus, HTE > Calu-3 > 16HBE14o- T84 > HFF = 0. A wide variety of neurohumoral agents and inflammatory stimuli was without effect on lactoferrin and lysozyme release from HTE or Calu-3 cells, although forskolin did stimulate secretion of water and lysozyme from Calu-3 cells. However, the concentration of lysozyme in the forskolin-induced secretions was much less than in airway gland secretions. Thus our data cast doubt on the utility of Calu-3 cells as a model of airway serous gland cells but do suggest that HTE could prove highly suitable for studies of mucin synthesis and release.

Adenocarcinoma↗
PubMed1990

Histamine stimulation of surfactant secretion from rat type II pneumocytes.

The present study examined the effect of histamine on the secretion of phosphatidylcholine, the predominant component of pulmonary surfactant from adult rat alveolar type II pneumocytes in primary culture. Histamine stimulated surfactant secretion in a time- and dose-dependent manner. At a concentration of 10 microM, histamine stimulated surfactant release by 5.2-fold over the basal secretory rate. The concentration producing half the maximal response for histamine-induced secretion was 70 nM. Histamine-induced secretion was blocked by both the selective histamine1 receptor antagonist pyrilamine and the selective histamine2 receptor antagonist cimetidine, but not by the beta-adrenergic antagonist alprenolol. Histamine activated adenylate cyclase and intracellular adenosine 3',5'-cyclic monophosphate (cAMP) production. These effects on adenylate cyclase and cAMP induced by histamine were inhibited by the H2 antagonist cimetidine. This would suggest that surfactant secretion was stimulated by histamine through H2 receptors and by cAMP. When histamine and isoproterenol were added concomitantly, the effects on phosphatidylcholine secretion were additive; however, there was no additive effect on adenylate cyclase activation. This coupled with H2 antagonist pyrilamine inhibition of histamine-induced secretion would suggest that histamine stimulated surfactant secretion through another mechanism in addition to a cAMP-dependent mechanism.

Adenylyl Cyclases↗
PubMed1984

A mechanistic model of ACTH-stimulated cortisol secretion.

Adrenal secretory rates of cortisol and arterial concentrations of adrenocorticotropin (ACTH) were measured in conscious trained dogs subjected to intravenous infusion of ACTH. To investigate the causal relation of ACTH to the secretion of cortisol, a mechanistic mathematical model based on current hypotheses of adrenocortical function was constructed and tested. It is widely believed that ACTH stimulates cortisol secretion through adenosine 3',5'-cyclic monophosphate (cAMP), which provides substrate cholesterol by activating cholesterol ester hydrolase and facilitating transport of cholesterol to the side-chain cleavage enzyme. In addition, cholesterol modulates its own synthesis by inhibiting beta-hydroxy-beta-methylglutaryl (HMG)-CoA reductase in the adrenocortical cell. These and other steps in the biosynthetic reaction sequence were described using differential equations subject to the additional constraints imposed by available measurements of intracellular quantities. The resulting model is consistent with many of the known characteristics of the canine adrenal response to ACTH. In this model, steady-state nonlinearities arise from cooperative binding of cAMP to its receptor protein and saturation of mitochondrial pregnenolone transport. The transient response is dominated by a depletable pool of intracellular free cholesterol. Other inferences based on the model are presented, and a quantifiable cellular basis for increased adrenal sensitivity to ACTH is proposed.

Adrenocorticotropic Hormone↗
PubMed1980

Renal renin responses to changes in volume status and perfusion pressure.

The effects on juxtaglomerular apparatus (JGA) renin activity of maneuvers known to acutely alter renin secretory rates were studied in rats. Five groups of rats were studied: group I: control; group II: 1% volume expansion; group III: 10% volume expansion; group IV: hypotensive hemorrhage; and group V: aortic clamping. Superficial (S) JGA renin activity was decreased in group II and further decreased in group III. Deep (D) JGA renin activity did not change. After hypotensive hemorrhage both S- and D-JGA renin activity increased. Similar results were seen after aortic clamping, although the increase in D-JGA renin activity was significantly less. These results indicate that S- and D-JGA renin activity may be under the control of different stimuli and may vary independently. They also support the concept that acute changes in renin secretion may be related to changes in renin synthesis.

Animals↗
PubMed1982

Renal Na+-K+-ATPase in renin release.

The effects of ouabain and furosemide on renin secretion, renal function, and renal Na+-K+-ATPase were investigated in anesthetized dogs. Furosemide (2 mg/kg) induced significant diuresis, natriuresis, an increase in renal blood flow (RBF), and a fivefold increase in renin secretory rate (RSR), but no changes in glomerular filtration rate (GFR). Infusion of ouabain (1 microgram . kg-1 . min-1) into one renal artery during furosemide diuresis increased fractional sodium excretion from 22 +/- 2 to 30 +/- 3% from the ipsilateral kidney but did not change urine flow, RBF, or GFR, whereas RSR fell to control values (698 +/- 203 to 137 +/- 43). When ouabain preceded furosemide, the rise in RBF and RSR induced by furosemide was abolished but sodium excretion increased. Ouabain infused in vivo inhibited Na+-K+-ATPase in microsomal fractions from cortex (34%) and medulla (27%) as compared with control. Neither saline nor furosemide exerted any effect on Na+-K+-ATPase. Moreover, the effect of ouabain alone on Na+-K+-ATPase was not different from that of ouabain plus furosemide. No changes in Mg2+-ATPase were detected in any of the experiments. These results indicate that inhibition of renal Na+-K+-ATPase abolishes furosemide-induced renin secretion despite potentiation of the natriuretic effect of the diuretic. It is apparent that the level of activity of Na+-K+-ATPase is of prime importance for renin secretion. In addition, ouabain may act directly on the juxtaglomerular cells to inhibit renin secretion.

Animals↗
PubMed1983

Secretion of tetraethylammonium by proximal tubules of rabbit kidneys.

The secretory transport of tetraethylammonium (TEA) was investigated in perfused and nonperfused isolated S1, S2, and S3 segments of proximal tubules from rabbit kidneys. In the perfused tubules the transepithelial net secretory flux and in nonperfused tubules the TEA cellular uptake were saturable (Km = 67 microM, Vmax = 2,480 fmol X min-1 X mm-1 in perfused S2 segments), energy dependent, and inhibited by mepiperphenidol. The net secretory flux of TEA (J b leads to j TEA) at a bath TEA concentration of 40 microM differed for the three segments and decreased in the order S1 greater than S2 greater than S3. The concentration of TEA in the perfusate leaving the tubule was approximately twice as great and the intracellular TEA concentration approximately 40 times as great as that in the bath. In nonperfused segments (40 microM TEA in the incubation medium) the TEA tissue water-to-medium ratio reached 100. In the three segments the ability to accumulate TEA across the peritubular membrane, thus, was similar, but the transepithelial secretory flux differed significantly. The differences in secretory rate between the three segments presumably result from differences in the luminal membrane permeability.

Animals↗
PubMed1989

Facilitation by serum albumin of renal tubular secretion of organic anions.

The role of albumin in tubular secretion of the organic anions p-aminohippurate (PAH, 21% albumin-bound at 1 microM) and methotrexate (MTX, 55% bound at 1 microM), and of the organic cation N1-methylnicotinamide (NMN, not bound), was investigated in isolated rabbit S2 proximal tubules. PAH or MTX secretory rates were low in the absence of colloids or in the presence of 1 g/dl dextran 40, and were reversibly two- to sevenfold stimulated by either 1 g/dl bovine (BSA, either regular, defatted, and/or dialyzed) or rabbit serum albumin, or by dialyzed native rabbit plasma. NMN secretion was not stimulated by either dextran or albumin. Luminal BSA had no effect, but stimulation of PAH secretion was observed when albumin was present in both lumen and bath. This secretion was BSA concentration-dependent up to a 1 g/dl BSA. Saturation experiments suggested that 1 g/dl BSA may increase PAH apparent affinity for secretion, with no change in its maximum velocity. Albumin appears therefore to facilitate organic anion proximal secretion by an effect unrelated to oncotic pressure or to the extent of organic anion binding.

Animals↗
PubMed2000

A mathematical model of the outer medullary collecting duct of the rat.

A mathematical model of the outer medullary collecting duct (OMCD) has been developed, consisting of alpha-intercalated cells and a paracellular pathway, and which includes Na(+), K(+), Cl(-), HCO(3)(-), CO(2), H(2)CO(3), phosphate, ammonia, and urea. Proton secretion across the luminal cell membrane is mediated by both H(+)-ATPase and H-K-ATPase, with fluxes through the H-K-ATPase given by a previously developed kinetic model (Weinstein AM. Am J Physiol Renal Physiol 274: F856-F867, 1998). The flux across each ATPase is substantial, and variation in abundance of either pump can be used to control OMCD proton secretion. In comparison with the H(+)-ATPase, flux through the H-K-ATPase is relatively insensitive to changes in lumen pH, so as luminal acidification proceeds, proton secretion shifts toward this pathway. Peritubular HCO(3)(-) exit is via a conductive pathway and via the Cl(-)/HCO(3)(-) exchanger, AE1. To represent AE1, a kinetic model has been developed based on transport studies obtained at 38 degrees C in red blood cells. (Gasbjerg PK, Knauf PA, and Brahm J. J Gen Physiol 108: 565-575, 1996; Knauf PA, Gasbjerg PK, and Brahm J. J Gen Physiol 108: 577-589, 1996). Model calculations indicate that if all of the chloride entry via AE1 recycles across a peritubular chloride channel and if this channel is anything other than highly selective for chloride, then it should conduct a substantial fraction of the bicarbonate exit. Since both luminal membrane proton pumps are sensitive to small changes in cytosolic pH, variation in density of either AE1 or peritubular anion conductance can modulate OMCD proton secretory rate. With respect to the OMCD in situ, available buffer is predicted to be abundant, including delivered HCO(3)(-) and HPO(4)(2-), as well as peritubular NH(3). Thus, buffer availability is unlikely to exert a regulatory role in total proton secretion by this tubule segment.

Acid-Base Equilibrium↗
PubMed1984

Autonomic regulation of viscoelasticity of cat tracheal gland secretions.

The purpose of this study was to determine whether various adrenergic agonists selectively regulate the viscoelastic properties of the stimulated secretions from airway submucosal glands. Nanoliter quantities of cat tracheal secretions before and during each of three stimuli were collected directly from a single submucosal gland with a micropipette, and the viscoelastic properties of the secretions were determined using a newly developed capillary microrheometer. Under unstimulated conditions (control), the measured values of apparent viscosity and elasticity of the secretions were more reproducible than the values obtained in previous studies in which samples were collected by other methods. After muscarinic (acetylcholine), alpha-adrenergic (phenylephrine), or beta-adrenergic (isoproterenol) stimulation, the submucosal gland's secretory rate was, in each case, greater than control. The viscoelastic properties of the secretions induced by muscarinic stimulation, however, were identical to control, whereas alpha-adrenergic stimulation produced secretions of a lower apparent viscosity, and beta-adrenergic stimulation produced secretions of a higher apparent viscosity and lower elasticity than control. Thus autonomic agonists selectively regulate the viscoelastic properties of submucosal gland secretions from cat trachea.

Acetylcholine↗
PubMed1986

Differential production of SRIF 14 and 28 by fetal rat hypothalamic cells enriched by velocity sedimentation.

Dispersed day-17 fetal rat hypothalamic cells have been enriched according to size by velocity sedimentation prior to culture, and the SRIF production by these enriched populations was compared with that of other enriched cell fractions and with mixed-cell cultures. Cultures of mixed cells produced 100-400 pg SRIF/10(6) cells/4 h over a period of 28 days. Total SRIF production by mixed cells was inversely proportional to seeding density over the range 0.25-1 X 10(6) cells/ml/well and SRIF 14 and 28 were secreted in a ratio of approximately 6:1. Although secretory rates by low cell densities remained higher than those by high cell densities, SRIF production decreased with time at all seeding densities (up to 21 days). Dispersed fetal hypothalamic cells were enriched according to size by allowing them to sediment over 4 h through a shallow gradient of BSA in culture medium and subsequent cell fractions developed widely differing morphologies in monolayer cultures. In contrast to mixed-cell cultures, SRIF production at 8 days by both large and small cells were directly proportional to initial seeding density. Furthermore, the smaller cells secreted very much less SRIF than the larger cells (100 pg/10(6) cells/4 h vs. 1,300 pg/10(6) cells/4 h), whereas there was little difference in overall SRIF content (350 pg/10(6) cells vs. 400 pg/10(6) cells). Characterisation by HPLC of the SRIF content and secretion of smaller cells revealed SRIF 14 to 28 ratios of 7:1 and 3:1, respectively. In contrast in the large cells, the ratio was 1:1 for both content and secretion. Therefore, these cell groups contain and secrete different proportions of these 2 molecular forms of SRIF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗