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.

Prolactin directly enhanced Na+/K+- and Ca2+-ATPase activities in the duodenum of female rats

2006 ◽  
Vol 84 (5) ◽  
pp. 555-563 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Liangchai Limlomwongse ◽  
Nateetip Krishnamra
Keyword(s):  
Atpase Activity ◽  
Brush Border ◽  
Calcium Transport ◽  
Calcium Uptake ◽  
Basolateral Membrane ◽  
Female Rats ◽  
Dependent Manner ◽  
Control Value ◽  
Crude Homogenate ◽  
Active Calcium

Prolactin has recently been shown to directly stimulate 2 components of the active duodenal calcium transport in female rats, i.e., solvent drag-induced and transcellular-active calcium transport. Since the basolateral Na+/K+- and Ca2+-ATPases, respectively, play important roles in these 2 transport mechanisms, the present study aimed to examine the direct actions of prolactin on the activities of both transporters in sexually mature female Wistar rats. The results showed that 200, 400, and 800 ng/mL prolactin produced a significant increase in the total ATPase activity of duodenal crude homogenate in a dose-dependent manner within 60 min (i.e., from a control value of 1.53 ± 0.13 to 2.29 ± 0.21 (p < 0.05), 2.68 ± 0.19 (p < 0.01), and 3.92 ± 0.33 (p < 0.001) µmol Pi·(mg protein)–1·min–1, respectively). Activity of Na+/K+-ATPase was increased by 800 ng/mL prolactin from 0.17 ± 0.03 to 1.18 ± 0.29 µmol Pi·(mg protein)–1·min–1 (p < 0.01). Prolactin at doses of 400 and 600 ng/mL also significantly increased the activities of Ca2+-ATPase in crude homogenate from a control value of 0.84 ± 0.03 to 1.75 ± 0.29 (p < 0.05), and 2.30 ± 0.37 (p < 0.001) µmol Pi·(mg protein)–1·min–1. When the crude homogenate was purified for the basolateral membrane, the Na+/K+-ATPase activities were elevated 10-fold. In the purified homogenate, 800 ng/mL prolactin increased Na+/K+-ATPase activity from 1.79 ± 0.38 to 2.63 ± 0.44 µmol Pi·(mg protein)–1·min–1 (p < 0.05), and Ca2+-ATPase activity from 0.08 ± 0.14 to 2.03 ± 0.23 µmol Pi·(mg protein)–1·min–1 (p < 0.001). Because the apical calcium entry was the first important step for the transcellular active calcium transport, the brush border calcium uptake was also investigated in this study. We found that, 8 min after being directly exposed to 800 ng/mL prolactin, the brush border calcium uptake into the duodenal epithelial cells was increased from 0.31 ± 0.02 to 0.80 ± 0.28 nmol·(mg protein)–1 (p < 0.05). It was concluded that prolactin directly and rapidly enhanced the brush border calcium uptake as well as the activities of the basolateral Na+/K+- and Ca2+-ATPases in the duodenal epithelium of female rats. These findings explained the mechanisms by which prolactin stimulated duodenal active calcium absorption.

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.

Chronic metabolic acidosis stimulated transcellular and solvent drag-induced calcium transport in the duodenum of female rats

2006 ◽  
Vol 291 (3) ◽  
pp. G446-G455 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Kukiat Tudpor ◽  
Naritsara Pulsook ◽  
Nateetip Krishnamra
Keyword(s):  
Metabolic Acidosis ◽  
Tight Junction ◽  
Mrna Expression ◽  
Calcium Transport ◽  
Female Rats ◽  
Calcium Balance ◽  
Solvent Drag ◽  
Chronic Metabolic Acidosis ◽  
Active Calcium ◽  
Relative Mrna Expression

Chronic metabolic acidosis results in a negative calcium balance as a result of bone resorption and renal calcium loss. However, reports on the changes in intestinal calcium transport have been controversial. The present investigation therefore aimed to study the effects of chronic metabolic acidosis induced by 1.5% NH4Cl administration on the three components of duodenal calcium transport, namely, solvent drag-induced, transcellular active, and passive paracellular components, in rats using an in vitro Ussing chamber technique. The relative mRNA expression of genes related to duodenal calcium transport was also determined. We found that 21-day chronic metabolic acidosis stimulated solvent drag-induced and transcellular active duodenal calcium transport but not passive paracellular calcium transport. Our results further demonstrated that an acute direct exposure to serosal acidic pH, in contrast, decreased solvent drag-induced calcium transport in a pH-dependent fashion but had no effect on transcellular active calcium transport. Neither the transepithelial resistance nor duodenal permeability to Na+, Cl−, and Ca2+ via the passive paracellular pathway were altered by chronic metabolic acidosis, suggesting that widening of the tight junction and changes in the charge-selective property of the tight junction did not occur. Thus the enhanced duodenal calcium transport observed in chronic metabolic acidosis could have resulted from a long-term adaptation, possibly at the molecular level. RT-PCR study revealed that chronic metabolic acidosis significantly increased the relative mRNA expression of duodenal genes associated with solvent drag-induced transport, i.e., the β1-subunit of Na+-K+-ATPase, zonula occludens-1, occludin, and claudin-3, and with transcellular active transport, i.e., transient receptor potential vanilloid family Ca2+ channels 5 and 6 and plasma membrane Ca2+-ATPase isoform 1b. Total plasma calcium and free ionized calcium and magnesium concentrations were also increased, whereas serum parathyroid hormone and 1α,25-dihydroxyvitamin D3 levels were not changed. The results indicated that 21-day chronic metabolic acidosis affected the calcium metabolism in rats partly through enhancing the mRNA expression of crucial duodenal genes involved in calcium absorption, thereby stimulating solvent drag-induced and transcellular active calcium transport in the duodenum.

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.

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.

AUGMENTATION BY CHLORMADINONE OF THE UTERINE WEIGHT RESPONSE TO HUMAN CHORIONIC GONADOTROPHIN IN INTACT IMMATURE RATS

1965 ◽  
Vol 33 (3) ◽  
pp. 447-454
Author(s):  
M. J. K. HARPER
Keyword(s):  
Single Injection ◽  
Direct Action ◽  
Follicular Development ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Female Rats ◽  
Uterine Weight ◽  
Control Value ◽  
Orally Active ◽  
Stimulation Of

SUMMARY Administration of chlormadinone, an orally active progestational agent without significant oestrogenic activity, to intact immature female rats did not affect either ovarian or uterine weight significantly compared with controls. A single injection of human chorionic gonadotrophin (HCG) caused a 73 % increase in uterine weight in 24 hr. over the control value. This dose significantly increased ovarian weight and although it caused some stimulation of follicular development, ovulation during this time did not occur. When animals were treated with chlormadinone for 8 days, and received HCG on the 8th day, uterine weight was 170% greater than in the controls and 56% greater than with HCG alone. The uterine weight produced was similar to that found in animals treated with mestranol, a potent oestrogen, and HCG. In ovariectomized animals HCG did not affect uterine weight, while the small increase produced by chlormadinone was unaltered when HCG also was given. Mechanisms are discussed by which this augmentation of the uterine response to HCG might be produced. It seems most likely that chlormadinone administration causes storage of endogenous gonadotrophin in the pituitary, and that the exogenous gonadotrophin acts as the 'trigger' for the release of stored hormone, probably by a direct action on the hypothalamus.

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.

scholarly journals 1,25-Dihydroxyvitamin D3 Rapidly Stimulates the Solvent Drag–Induced Paracellular Calcium Transport in the Duodenum of Female Rats

2008 ◽  
Vol 58 (5) ◽  
pp. 297-307 ◽  
Author(s):  
Kukiat Tudpor ◽  
Jarinthorn Teerapornpuntakit ◽  
Walailuk Jantarajit ◽  
Nateetip Krishnamra ◽  
Narattaphol Charoenphandhu
Keyword(s):  
Calcium Transport ◽  
Female Rats ◽  
Solvent Drag ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3

Calcium transport in small intestine during pregnancy and lactation

1980 ◽  
Vol 239 (1) ◽  
pp. E64-E68 ◽  
Author(s):  
B. P. Halloran ◽  
H. F. DeLuca
Keyword(s):  
Vitamin D ◽  
Reproductive Cycle ◽  
Calcium Transport ◽  
Plasma Concentrations ◽  
Dihydroxyvitamin D ◽  
Control Value ◽  
1,25 Dihydroxyvitamin D ◽  
Everted Gut Sac ◽  
Pregnancy And Lactation ◽  
Active Calcium

The factors involved in calcium homeostasis during the mammalian reproductive cycle and specifically in the control of active calcium transport in the intestine have not been thoroughly investigated. For this reason calcium transport in the intestine was measured in vitamin D-replete and vitamin D-deficient rats during pregnancy and lactation using the everted gut sac technique. In addition the changes in the plasma concentrations of calcium and 1,25-dihydroxyvitamin D were measured and correlated with transport. During the later stages of pregnancy and during lactation, the concentration of calcium in the plasma is reduced 10-30%. In turn, in the vitamin D-replete rat, the concentration of 1,25-dihydroxyvitamin D in the plasma increases from a control value of 26 pg/ml to 158 pg/ml at day 14 of lactation. Calcium transport in the intestine increases late in pregnancy, peaks during lactation, and then falls to control values by 3 wk postweaning in both vitamin D-replete and D-deficient animals. These findings strengthen the established relationship between 1,25-dihydroxyvitamin D and active calcium transport in the intestine as well as suggest that some factor(s) independent of vitamin D is stimulating intestinal calcium transport during the reproductive cycle.

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