scholarly journals Calcium Absorption by the Midgut of the Blowfly, Calliphora Vicina

1985 ◽  
Vol 114 (1) ◽  
pp. 551-561 ◽  
Author(s):  
Colin W. Taylor
Keyword(s):  
Calcium Transport ◽  
Calcium Absorption ◽  
Water Flux ◽  
Calcium Flux ◽  
Calliphora Vicina ◽  
Internal Perfusion ◽  
Electrochemical Gradient ◽  
Saturation Kinetics ◽  
Active Calcium ◽  
Net Water Flux

The isolated midgut of the adult blowfly, Calliphora vicina, can be maintained under internal perfusion for over 6h, and calcium absorption measured by including 45Ca in the perfusing saline with [3H[inulin as a volume marker. The midgut has a considerable capacity to transport calcium from the lumen (L) to the bathing saline (BS) against its electrochemical gradient and in the absence of an appreciable net water flux across the gut. Calcium absorption (L-BS) shows saturation kinetics, is totally and reversibly inhibited by metabolic poisons and is accompanied by a negligible backflux (BS-L). It is concluded that the midgut of C. vicina is capable of active calcium transport and that the entire transepithelial calcium flux occurs via a transcellular route. This contrasts with the mammalian duodenum, where absorption occurs via a combination of transcellular and paracellular routes.

Glucose enhancement of transcellular calcium transport in the intestine

1988 ◽  
Vol 255 (3) ◽  
pp. G339-G345 ◽  
Author(s):  
K. M. Carroll ◽  
R. J. Wood ◽  
E. B. Chang ◽  
I. H. Rosenberg
Keyword(s):  
Calcium Transport ◽  
Calcium Uptake ◽  
Calcium Absorption ◽  
Membrane Integrity ◽  
Calcium Flux ◽  
Calcium Efflux ◽  
Cell Membrane Integrity ◽  
Active Calcium ◽  
Altered Cell

Glucose stimulates calcium transport in vitro in rat duodenal tissue and isolated enterocytes. Under short-circuited conditions, glucose increased mucosal to serosal calcium flux (JCa(m----s)) without altering serosal to mucosal calcium flux (JCa(s----m)) in the duodenum, the primary site of active calcium absorption in the rat small intestine. The half-maximal dose (ED50) of the glucose stimulatory effect was less than 1 mM, and an increase in JCa(m----s) of 80% over control was seen at a glucose concentration of 50 mM. Glucose did not increase calcium flux in the ileum where active calcium absorption is minimal. Glucose stimulated net calcium uptake by 35% in isolated duodenal enterocytes. Glucose did not alter calcium efflux from preloaded enterocytes suspended in calcium-free buffer. Glucose enhancement of net calcium uptake in enterocytes was not caused by altered cell membrane integrity or functional viability. The nonmetabolizable glucose analogue alpha-methylglucoside did not stimulate calcium transport. Our findings suggest that glucose can stimulate intestinal calcium absorption, at least partially, by enhancing transcellular calcium transport and that cellular glucose metabolism is necessary for stimulation of this route of calcium transport.

Prolactin directly stimulates transcellular active calcium transport in the duodenum of female rats

2001 ◽  
Vol 79 (5) ◽  
pp. 430-438 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Liangchai Limlomwongse ◽  
Nateetip Krishnamra
Keyword(s):  
Calcium Transport ◽  
Calcium Absorption ◽  
Direct Action ◽  
Female Rats ◽  
Calcium Flux ◽  
Total Calcium ◽  
Solvent Drag ◽  
Control Value ◽  
Voltage Dependent ◽  
Active Calcium

Prolactin has been postulated to be a novel calcium-regulating hormone during pregnancy and lactation. It stimulates both passive and active duodenal calcium transport in several experimental models. Our study was performed on sexually mature female Wistar rats (200–250 g) to study the direct action of prolactin on calcium transport in the duodenum using the Ussing chamber technique. To evaluate the effect of prolactin on total calcium transport in the duodenum, we intraperitoneally injected rats with 0.4, 0.6, and 0.8 mg/kg prolactin. The total calcium transport was divided into voltage-dependent, solvent drag-induced, and transcellular active fluxes by applying short-circuit current and by mucosal glucose replacement with mannitol. The effect of prolactin on each flux was studied separately. Finally, to evaluate the direct action of prolactin on duodenal transcellular active flux, we directly exposed duodenal segments to prolactin that had been added to the serosal solution with or without calcium transport inhibitors. We found that 0.6 and 0.8 mg/kg prolactin ip significantly increased the total mucosa–to–serosa calcium flux from the control value (nmol·hr–1·cm–2) of 34.53 ± 6.81 to 68.07 ± 13.53 (P < 0.05) and 84.43 ± 19.72 (P < 0.01), respectively. Prolactin also enhanced the solvent drag-induced calcium flux and transcellular active calcium flux, but not the voltage-dependent calcium flux. The duodenal segments directly exposed to 200, 400, and 800 ng/mL prolactin showed a significant increase in the transcellular active calcium absorption in a dose-dependent manner, i.e., from the control value (nmol·hr–1·cm–2) of 2.94 ± 0.47 to 5.45 ± 0.97 (P < 0.01), 8.09 ± 0.52 (P < 0.001), and 18.42 ± 2.92 (P < 0.001), respectively. Its direct action was inhibited by mucosal exposure to 50 µM lanthanum chloride, a calcium transporter protein competitor, and serosal exposure to 0.1 mM trifluoperazine, a Ca2+-ATPase inhibitor. These studies demonstrate that the duodenum is a target organ of prolactin, which enhances transcellular active calcium transport.Key words: calcium absorption, duodenum, prolactin, solvent drag, transcellular calcium transport.

Calcium transport in turtle bladder

1987 ◽  
Vol 253 (6) ◽  
pp. R917-R921
Author(s):  
S. Sabatini ◽  
N. A. Kurtzman
Keyword(s):  
Calcium Transport ◽  
Calcium Absorption ◽  
Short Circuit ◽  
Open Circuit ◽  
Calcium Flux ◽  
Bladder Epithelium ◽  
Control Value ◽  
Sodium Calcium ◽  
Turtle Bladder ◽  
Absorptive Flux

Unidirectional 45Ca fluxes were measured in the turtle bladder under open-circuit and short-circuit conditions. In the open-circuited state net calcium flux (JnetCa) was secretory (serosa to mucosa) and was 388.3 +/- 84.5 pmol.mg-1.h-1 (n = 20, P less than 0.001). Ouabain (5 X 10(-4) M) reversed JnetCa to an absorptive flux (serosal minus mucosal flux = -195.8 +/- 41.3 pmol.mg-1.h-1; n = 20, P less than 0.001). Amiloride (1 X 10(-5) M) reduced both fluxes such that JnetCa was not significantly different from zero. Removal of mucosal sodium caused net calcium absorption; removal of serosal sodium caused calcium secretion. When bladders were short circuited, JnetCa decreased to approximately one-third of control value but remained secretory (138.4 +/- 54.3 pmol.mg-1.h-1; n = 9, P less than 0.025). When ouabain was added under short-circuit conditions, JnetCa was similar in magnitude and direction to ouabain under open-circuited conditions (i.e., absorptive). Tissue 45Ca content was approximately equal to 30-fold lower when the isotope was placed in the mucosal bath, suggesting that the apical membrane is the resistance barrier to calcium transport. The results obtained in this study are best explained by postulating a Ca2+-ATPase on the serosa of the turtle bladder epithelium and a sodium-calcium antiporter on the mucosa. In this model, the energy for calcium movement would be supplied, in large part, by the Na+-K+-ATPase. By increasing cell sodium, ouabain would decrease the activity of the mucosal sodium-calcium exchanger (or reverse it), uncovering active calcium transport across the serosa.

Active calcium transport in the skin of the frog Rana pipiens: kinetics and seasonal rhythms.

1995 ◽  
Vol 198 (4) ◽  
pp. 967-974
Author(s):  
D F Stiffler
Keyword(s):  
Calcium Transport ◽  
Rana Pipiens ◽  
Dorsal Skin ◽  
Electrochemical Gradient ◽  
Fish Gill ◽  
Seasonal Rhythms ◽  
Active Calcium ◽  
Net Flux ◽  
Ventral Skin ◽  
Freshwater Environments

The frog Rana pipiens takes up Ca2+ against an electrochemical gradient from dilute external solutions that are similar to natural freshwater environments. The influx is dependent upon external [Ca2+] and is saturable. Kinetic analysis yielded a Km of 0.625 mmol l-1 and a Jmax of 38 nmol cm-2h-1. These kinetic variables suggest that both the affinity and capacity are smaller than those for Na+ and Cl- transport in the skin of the same species. They are also smaller than those for Ca2+ transport in fish gill. A significant portion (20-25%) of the Ca2+ entering a frog remains in Ca(2+)-rich layers of the skin, with ventral skin containing about three times as much Ca2+ as dorsal skin. There are seasonal rhythms in Ca2+ exchange: although Ca2+ influx does not vary significantly over the year, efflux is minimal in July, while net flux, which is negative most of the year, appears to be positive in July. Since these fluxes do not include dietary calcium, one cannot conclude that feeding frogs are in negative Ca2+ balance.

Ca fluxes across duodenum and colon of spontaneously hypertensive rats: effect of 1,25(OH)2D3

1986 ◽  
Vol 251 (2) ◽  
pp. F278-F282 ◽  
Author(s):  
U. Gafter ◽  
S. Kathpalia ◽  
D. Zikos ◽  
K. Lau
Keyword(s):  
Calcium Transport ◽  
Spontaneously Hypertensive Rats ◽  
Calcium Absorption ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Calcium Flux ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Calcium absorption by spontaneously hypertensive rats (SHR) was variably reported to be different from normotensive Wistar-Kyoto (WKY) controls. Furthermore, blunted responsiveness to the intestinal effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] has also been postulated. To evaluate this hypothesis, calcium fluxes were measured by the Ussing technique across duodenum and descending colon with or without prior 1,25(OH)2D3 treatment. Duodenal mucosal-to-serosal calcium flux (Jm----s) (44.9 vs. 52.4 nmol X cm-2 X h-1), serosal-to-mucosal flux (Js----m) (25.6 vs. 28.4 nmol X cm-2 X h-1), and net flux (Jnet) were comparable. 1,25(OH)2D3 increased duodenal Jm----s in both SHR and WKY groups (95.2 and 86.8 nmol X cm-2 X h-1). Js----m was lower in SHR (26.1 vs. 35.6 nmol X cm-2 X h-1, P less than 0.01), although the tendency for a higher Jnet in SHR (68.6 vs. 51.2 nmoles X cm-2 X h-1) was statistically insignificant. Short-circuit current was higher in the colon of SHR, both before and after 1,25(OH)2D3, suggesting increased sodium transport. Basal colonic Jnet was virtually zero in both groups but comparably increased by 1,25(OH)2D3 because of stimulation in only Jm----s. Prevention of hypertension by hydralazine since the 4th wk of age did not alter the findings compared with the hypertensive SHR, suggesting calcium transport rates were unaffected by hypertension. These data indicate that in vitro, duodenal, and colonic active calcium transport by the SHR is similar to WKY. Their normal responses to 1,25(OH)2D3 do not support the hypothesis of intestinal resistance.

Voltage dependence of calcium transport in the thick ascending limb of Henle's loop

1979 ◽  
Vol 236 (4) ◽  
pp. F357-F364 ◽  
Author(s):  
J. E. Bourdeau ◽  
M. B. Burg
Keyword(s):  
Calcium Transport ◽  
Calcium Absorption ◽  
Calcium Flux ◽  
Thick Ascending Limb ◽  
Sodium Permeability ◽  
Calcium Fluxes ◽  
Henle's Loop ◽  
Wide Range ◽  
Net Flux

Thick ascending limbs of Henle's loop were dissected from rabbit kidneys and perfused in vitro. Unidirectional transepithelial calcium fluxes from lumen-to-bath and bath-to-lumen were measured with 45Ca using different solutions that caused the transepithelial voltage to vary over a wide range. With lumen-positive voltages there was net calcium absorption from lumen to bath which varied directly with the voltage. With voltage near zero there was no measurable net flux. When the voltage was made negative, the direction of net calcium transport reversed (i.e., secretion from bath to lumen). The presence or absence of bicarbonate in the lumen did not affect the calcium fluxes. Calcium permeability, calculated from the dependence of net flux on voltage, was 7.7 x 10(-6) cm/s, which is approximately 25% of the sodium permeability previously determined in this segment. Analysis of the calcium flux ratios revealed interdependence of the bidirectional fluxes consistent with single-file diffusion but no evidence for active calcium transport. We conclude that there is an important component of passive net calcium transport driven by the voltage in this segment.

Effect of aluminum on bidirectional calcium flux in rat everted intestinal sacs

1989 ◽  
Vol 257 (3) ◽  
pp. G433-G437
Author(s):  
A. J. Adler ◽  
C. Zara ◽  
G. M. Berlyne
Keyword(s):  
Glucose Transport ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Calcium Flux ◽  
Serosal Side ◽  
Active Process ◽  
Sprague Dawley ◽  
Calcium Isotopes ◽  
Sprague Dawley Rats ◽  
Ambient Concentrations

The effect of aluminum on intestinal calcium absorption was determined in male Sprague-Dawley rats using an everted intestinal sac technique. Bidirectional calcium flux in the duodena and ilea of normal rats was assessed by means of dual calcium isotopes. Two micromolar aluminum significantly inhibited net calcium absorption (J net) in the duodenum through suppression of mucosato-serosa flux (J m----s). Jm----s was reduced from 2.21 +/- 0.50 mumol Ca.h-1.g wet wt-1 in controls to 0.93 +/- 0.35 mumol Ca.h-1.g-1 in aluminum exposed sacs, and Jnet was reduced from 1.88 +/- 0.14 mumol Ca.h-1.g-1 to 0.55 +/- 0.41 mumol Ca.h-1.g-1 (P less than 0.001). Serosa-to-mucosa calcium flux (Js----m) was not similarly influenced by aluminum. Inhibition of Jm----s occurred whether aluminum was initially present on the mucosal or serosal side of the duodenal sac and inhibition of Jnet calcium by 2 muM A1 occurred at all ambient concentrations of calcium studied. In the ileum, aluminum had no effect on any component of calcium flux. Aluminum did not induce any suppression of glucose transport in either the duodenum or ileum, suggesting that the effect on calcium transport is relatively specific. These results suggest that aluminum inhibits calcium absorption in the duodenum through an effect on active mucosa-to-serosa transport, but has no effect on ileal calcium absorption, which in the rat is not mediated by an active process.

Enhancement of calcium transport in Caco-2 monolayer through PKCζ-dependent Cav1.3-mediated transcellular and rectifying paracellular pathways by prolactin

2009 ◽  
Vol 296 (6) ◽  
pp. C1373-C1382 ◽  
Author(s):  
Narongrit Thongon ◽  
La-iad Nakkrasae ◽  
Jirawan Thongbunchoo ◽  
Nateetip Krishnamra ◽  
Narattaphol Charoenphandhu
Keyword(s):  
Protein Kinase ◽  
Calcium Channel ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Protein Biosynthesis ◽  
Ussing Chamber ◽  
Calcium Flux ◽  
Channel Blockers ◽  
Voltage Dependent ◽  
Calbindin D

Previous investigations suggested that prolactin (PRL) stimulated the intestinal calcium absorption through phosphoinositide 3-kinase (PI3K), protein kinase C (PKC), and RhoA-associated coiled-coil forming kinase (ROCK) signaling pathways. However, little was known regarding its detailed mechanisms for the stimulation of transcellular and voltage-dependent paracellular calcium transport. By using Ussing chamber technique, we found that the PRL-induced increase in the transcellular calcium flux and decrease in transepithelial resistance of intestinal-like Caco-2 monolayer were not abolished by inhibitors of gene transcription and protein biosynthesis. The PRL-stimulated transcellular calcium transport was completely inhibited by the L-type calcium channel blockers (nifedipine and verapamil) and plasma membrane Ca2+-ATPase (PMCA) inhibitor (trifluoperazine) as well as small interfering RNA targeting voltage-dependent L-type calcium channel Cav1.3, but not TRPV6 or calbindin-D9k. As demonstrated by 45Ca uptake study, PI3K and PKC, but not ROCK, were essential for the PRL-enhanced apical calcium entry. In addition, PRL was unable to enhance the transcellular calcium transport after PKCζ knockdown or exposure to inhibitors of PKCζ, but not of PKCα, PKCβ, PKCε, PKCμ, or protein kinase A. Voltage-clamping experiments further showed that PRL markedly stimulated the voltage-dependent calcium transport and removed the paracellular rectification. Such PRL effects on paracellular transport were completely abolished by inhibitors of PI3K (LY-294002) and ROCK (Y-27632). It could be concluded that the PRL-stimulated transcellular calcium transport in Caco-2 monolayer was mediated by Cav1.3 and PMCA, presumably through PI3K and PKCζ pathways, while the enhanced voltage-dependent calcium transport occurred through PI3K and ROCK pathways.

Influence of vitamin D on calcium absorption in the chick

1962 ◽  
Vol 203 (3) ◽  
pp. 497-505 ◽  
Author(s):  
J. D. Sallis ◽  
E. S. Holdsworth
Keyword(s):  
Vitamin D ◽  
Small Intestine ◽  
Calcium Transport ◽  
Calcium Absorption ◽  
Metabolic Inhibitors ◽  
Hydroxyl Groups ◽  
Oxidation Reduction ◽  
Active Calcium

The site of absorption of Ca45 was studied in rachitic chicks and rachitic chicks given vitamin D3. Vitamin D3 markedly increases absorption from the small intestine and, in vivo, similar amounts of calcium are absorbed along the entire small intestine. With everted gut sacs, the distal third of the small intestine transported much more calcium than did the duodenal and middle sections. Thus, interpretations of in vitro results may not always depict the natural in vivo process. Vitamin D2 had little activity in the chick, but AT-10 series 2 and AT-10 series 3 were almost as active as vitamin D3 for calcium transport. These results suggest an "active carrier" may be formed by addition of hydrogen or hydroxyl groups to the opened ring B of vitamin D, giving a carrier capable of reversible oxidation-reduction or keto-enol tautomerism. Using metabolic inhibitors, active calcium transport in vitro relied on glycolysis for its energy supply. The transport was independent of the sodium pump.

Net Fluxes of Water in the Isolated Gills of Anguilla Dieffenbachii

1974 ◽  
Vol 60 (3) ◽  
pp. 769-781
Author(s):  
T. J. SHUTTLEWORTH ◽  
R. F. H. FREEMAN
Keyword(s):  
Sea Water ◽  
Water Flux ◽  
Freshwater Teleost ◽  
Osmotic Permeability ◽  
Direct Measurements ◽  
Net Flux ◽  
Anguilla Dieffenbachii ◽  
Net Fluxes ◽  
Freshwater Eels ◽  
Net Water Flux

1. Measurements of net flux of water have been made on isolated gills removed from freshwater-adapted and seawater-adapted eels and incubated in various media of differing osmotic pressure. 2. From these measurements it has been possible to determine the osmotic permeability coefficient of the gill directly from the net water flux. The values obtained (0.50±0.14x10-5 cm.sec-1 for freshwater eels and 0.43±0.07x10-5 cm.sec-1 for seawater-adapted eels) indicate that there was no significant change in this parameter on adaptation of the eels to sea water. 3. The direct measurements made of the net water flux across the isolated gills appear to be compatible with the osmoregulatory pattern of eels as deduced by other workers using different techniques. In particular they illustrate and further emphasize the significance of drinking in the freshwater fish. 4. Calculations indicate that, for a freshwater teleost, the osmotic and ionic problems caused by drinking in fresh water have an insignificant energetic effect and hence, energetically, it matters little to the fish whether it drinks or not.

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