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.

Chronic metabolic acidosis upregulated claudin mRNA expression in the duodenal enterocytes of female rats

Life Sciences ◽  
2007 ◽  
Vol 80 (19) ◽  
pp. 1729-1737 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Kannikar Wongdee ◽  
Kukiat Tudpor ◽  
Jantarima Pandaranandaka ◽  
Nateetip Krishnamra
Keyword(s):  
Metabolic Acidosis ◽  
Mrna Expression ◽  
Female Rats ◽  
Chronic Metabolic Acidosis

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.

scholarly journals Carbonic anhydrase II and IV mRNA in rabbit nephron segments: stimulation during metabolic acidosis

1998 ◽  
Vol 274 (2) ◽  
pp. F259-F267 ◽  
Author(s):  
Shuichi Tsuruoka ◽  
Ann M. Kittelberger ◽  
George J. Schwartz
Keyword(s):  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Mrna Expression ◽  
Collecting Duct ◽  
Proximal Tubules ◽  
Rabbit Kidney ◽  
Rt Pcr ◽  
Chronic Metabolic Acidosis ◽  
Nephron Segments ◽  
Medullary Collecting Duct

Carbonic anhydrase (CA) facilitates renal bicarbonate reabsorption and acid excretion. Cytosolic CA II catalyzes the buffering of intracellular hydroxyl ions by CO2, whereas membrane-bound CA IV catalyzes the dehydration of carbonic acid generated from the secretion of protons. Although CA II and IV are expressed in rabbit kidney, it is not entirely clear which segments express which isoforms. It was the purpose of this study to characterize the expression of CA II and CA IV mRNAs by specific segments of the nephron using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and to determine the effect of chronic metabolic acidosis on CA expression by those segments. Individual nephron segments (usually 1–2 mm) were isolated by microdissection and subjected to RT-PCR. Amplification was performed simultaneously for CA IV, CA II, and malate dehydrogenase (MDH), a housekeeping gene. The intensities of the PCR products were quantitated by densitometry. CA IV mRNA was expressed by S1 and S2 proximal tubules and by outer medullary collecting duct from inner stripe (OMCDi) and outer stripe and initial inner medullary collecting duct (IMCDi). CA II mRNA was expressed by S1, S2, and S3 proximal tubules, thin descending limb, connecting segment (CNT), and all collecting duct segments. Acid loading induced CA IV mRNA expression in S1 and S2 proximal tubules and in OMCDi and IMCDi. CA II mRNA was induced by acidosis in all three proximal segments and nearly all distal segments beginning with CNT. No upregulation of MDH mRNA expression occurred. These adaptive increases in CA II and IV mRNAs are potentially important in the kidney’s adaptation to chronic metabolic acidosis.

Renal expression of the ammonia transporters, Rhbg and Rhcg, in response to chronic metabolic acidosis

2006 ◽  
Vol 290 (2) ◽  
pp. F397-F408 ◽  
Author(s):  
Ramanathan M. Seshadri ◽  
Janet D. Klein ◽  
Shelley Kozlowski ◽  
Jeff M. Sands ◽  
Young-Hee Kim ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Protein Expression ◽  
Mrna Expression ◽  
Collecting Duct ◽  
Broad Band ◽  
Ammonia Excretion ◽  
Intercalated Cells ◽  
Outer Medulla ◽  
Chronic Metabolic Acidosis ◽  
Medullary Collecting Duct

Chronic metabolic acidosis induces dramatic increases in net acid excretion that are predominantly due to increases in urinary ammonia excretion. The current study examines whether this increase is associated with changes in the expression of the renal ammonia transporter family members, Rh B glycoprotein (Rhbg) and Rh C glycoprotein (Rhcg). Chronic metabolic acidosis was induced in Sprague-Dawley rats by HCl ingestion for 1 wk; control animals were pair-fed. After 1 wk, metabolic acidosis had developed, and urinary ammonia excretion increased significantly. Rhcg protein expression was increased in both the outer medulla and the base of the inner medulla. Intercalated cells in the outer medullary collecting duct (OMCD) and in the inner medullary collecting duct (IMCD) in acid-loaded animals protruded into the tubule lumen and had a sharp, discrete band of apical Rhcg immunoreactivity, compared with a flatter cell profile and a broad band of apical immunolabel in control kidneys. In addition, basolateral Rhcg immunoreactivity was observed in both control and acidotic kidneys. Cortical Rhcg protein expression and immunoreactivity were not detectably altered. Rhcg mRNA expression was not significantly altered in the cortex, outer medulla, or inner medulla by chronic metabolic acidosis. Rhbg protein and mRNA expression were unchanged in the cortex, outer and inner medulla, and no changes in Rhbg immunolabel were evident in these regions. We conclude that chronic metabolic acidosis increases Rhcg protein expression in intercalated cells in the OMCD and in the IMCD, where it is likely to mediate an important role in the increased urinary ammonia excretion.

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

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.

scholarly journals Prolactin directly stimulated the solvent drag-induced calcium transport in the duodenum of female rats

2004 ◽  
Vol 1665 (1-2) ◽  
pp. 81-91 ◽  
Author(s):  
Chaiyot Tanrattana ◽  
Narattaphol Charoenphandhu ◽  
Liangchai Limlomwongse ◽  
Nateetip Krishnamra
Keyword(s):  
Calcium Transport ◽  
Female Rats ◽  
Solvent Drag

Vitamin D and Magnesium Absorption in Man

1979 ◽  
Vol 57 (1) ◽  
pp. 121-123 ◽  
Author(s):  
A. Hodgkinson ◽  
D. H. Marshall ◽  
B. E. C. Nordin
Keyword(s):  
Vitamin D ◽  
Calcium Transport ◽  
Alkaline Earth ◽  
Calcium Balance ◽  
Slight Effect ◽  
Strontium Barium ◽  
Active Calcium ◽  
The Mean ◽  
Calcium And Magnesium ◽  
Stimulation Of

1. The effects of vitamin D and its hydroxylated derivatives on calcium and magnesium absorption have been examined in 47 balance studies on patients with various disorders of calcium or bone metabolism. 2. Vitamin D significantly increased the mean net absorption of calcium and also the calcium balance. The mean net absorption of magnesium was also significantly increased although the rise was much less than that of calcium and the mean magnesium balance was unaffected. 3. It is suggested that the slight effect of vitamin D on magnesium absorption may be incidental to its stimulation of active calcium transport, since the latter system has weak affinities for other alkaline earth ions including strontium, barium and magnesium.

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