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G Giebisch - One of the best experts on this subject based on the ideXlab platform.
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bicarbonate transport along the Loop of Henle molecular mechanisms and regulation
Journal of Nephrology, 2002Co-Authors: Giovambattista Capasso, Robert J Unwin, Maria Rosaria Rizzo, A Pica, G GiebischAbstract:The Loop of Henle (LOH) is an important site of renal tubule acidification. A combination of several techniques, including in vivo microperfusion, perfusion in vitro of the S3 segment of the proximal tubule and of the thick ascending limb (TAL) of Henle's Loop, as well as quantitative PCR performed on isolated TAL, has permitted the definition of key transporters and their role in modulating bicarbonate reabsorption in physiological and pathophysiological conditions. Na(+)-H+ exchange is the most important transport mechanism responsible for bicarbonate reabsorption, although a small but significant contribution of H(+)-ATPase-mediated bicarbonate reabsorption can also be identified. NHE3 is the main of several NHE isoforms expressed in the TAL and in the S3 segment of the proximal tubule. Special properties of the Na(+)-H+ exchanger in the TAL are its relative insensitivity to changes in cell pH (pHi) and the tight coupling between apical and basolateral Na(+)-H+ exchange. Several hormones, including anti-diuretic hormone (ADH), angiotensin II (AII), and gluco- and mineralocorticoids regulate Na(+)-H+ exchange. Loop diuretics such as furosemide stimulate bicarbonate transport along the LOH. Systemic acid-base disturbances also modulate bicarbonate transport: acidosis increases bicarbonate reabsorption, while metabolic alkalosis has the opposite effect. Neither hypokalemic alkalosis nor respiratory alkalosis or respiratory acidosis alter bicarbonate transport along the LOH. A significant role of HCO3 backflux, most likely through the paracellular pathway of the TAL, can also be observed. Changes in extracellular osmolality also affect bicarbonate reabsorption: hypertonicity inhibits, whereas hypotonicity stimulates transport. Transport activation is also observed as an adaptive response to glomerular hyperfiltration.
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localization of diuretic effects along the Loop of Henle an in vivo microperfusion study in rats
Clinical Science, 2000Co-Authors: R Unwin, G Giebisch, Giovambattista Capasso, S J Walter, David G ShirleyAbstract:In order to clarify the effects on sodium reabsorption in the Loop of Henle of methazolamide (a carbonic anhydrase inhibitor), chlorothiazide and the Loop diuretics frusemide and bumetanide, superficial Loops were perfused in vivo in anaesthetized rats and the individual diuretics were included in the perfusate. Differentiation between effects in the pars recta and in the thick ascending limb of Henle (TALH) was achieved by comparing responses to the diuretics when using a standard perfusate, designed to mimic native late proximal tubular fluid, and a low-sodium perfusate, designed to block net sodium reabsorption in the pars recta. With the standard perfusate, methazolamide caused decreases in sodium reabsorption (J(Na)) and water reabsorption (J(V)); with the low-sodium perfusate, a modest effect on J(Na) persisted, suggesting that carbonic anhydrase inhibition reduces sodium reabsorption in both the pars recta and the TALH. The effects of chlorothiazide were very similar to those of methazolamide with both the standard and low-sodium perfusates, suggesting that chlorothiazide also inhibits sodium reabsorption in the pars recta and TALH, perhaps through inhibition of carbonic anhydrase. With the standard perfusate, both frusemide and bumetanide produced the expected large decreases in J(Na), but J(V) was also lowered. With the low-sodium perfusate, the inhibitory effects of the Loop diuretics, particularly those of frusemide, were substantially reduced, while net potassium secretion was found. These observations indicate that a significant component of the effect of frusemide (and possibly of bumetanide) on overall sodium reabsorption is located in the pars recta, and that Loop diuretics induce potassium secretion in the TALH.
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contribution of na h exchange to sodium reabsorption in the Loop of Henle a microperfusion study in rats
The Journal of Physiology, 1998Co-Authors: D G Shirley, Robert J Unwin, S J Walter, G GiebischAbstract:1The contribution of apical Na+-H+ exchange to sodium reabsorption in the thick ascending limb of the Loop of Henle (TALH) in vivo was examined in anaesthetized rats by perfusing Loops of Henle of superficial nephrons with solutions containing the Na+-H+ exchange inhibitor, ethyl isopropyl amiloride (EIPA). 2Using a standard perfusate, no statistically significant effect of EIPA on net sodium reabsorption (JNa) was detected. However, when sodium reabsorption in the pars recta of the proximal tubule was minimized by using a low-sodium perfusate, EIPA reduced JNa from 828 ± 41 to 726 ± 37 pmol min−1 (P < 0.05), indicating that apical Na+-H+ exchange can make a small contribution to net sodium reabsorption in the TALH in vivo. This contribution appears to be dependent on the bicarbonate load, since an increase in the latter led to an enhancement of EIPA-sensitive sodium transport. 3Addition of the Na+-K+-2Cl− cotransport inhibitor, bumetanide, to the low-sodium perfusate reduced baseline JNa to 86 ± 27 pmol min−1. In this setting, EIPA reduced JNa further, to −24 ± 18 pmol min−1 (P < 0.05), an effect similar to that seen in the absence of bumetanide. This finding argues against previous suggestions (based on in vitro evidence) that inhibition of the Na+-K+-2Cl− cotransporter leads to an increase in apical Na+-H+ exchange in the TALH.
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bicarbonate transport along the Loop of Henle effects of adrenal steroids
American Journal of Physiology-renal Physiology, 1995Co-Authors: Robert Unwin, Giovambattista Capasso, G GiebischAbstract:The role of adrenal steroids in the regulation of bicarbonate absorption in the Loop of Henle was studied by in vivo microperfusion. Bicarbonate transport (JHCO3) was measured by microcalorimetry and fluid reabsorption by [14C]inulin, 7-10 days after surgery, in 1) sham-operated control rats, 2) adrenalectomized (Adx) rats, 3) Adx rats receiving dexamethasone (1.2 micrograms.100 g body wt-1.24 h-1) and a low dose of aldosterone (0.5 micrograms.100 g body wt-1.24 h-1), 4) Adx rats receiving dexamethasone, 5) Adx rats receiving a low dose of aldosterone, and 6) Adx rats receiving a high dose of aldosterone (1.0 micrograms.100 g body wt-1.24 h-1). JHCO3 along the Loop of Henle was decreased by 40% in Adx rats. JHCO3 was increased by dexamethasone alone and by dexamethasone plus a low dose of aldosterone to rates observed in fully supplemented Adx rats. Aldosterone given alone at a low physiological dose had no effect, but, when administered at a high dose, returned JHCO3 to normal.
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potassium and sodium transport along the Loop of Henle effects of altered dietary potassium intake
Kidney International, 1994Co-Authors: Robert Unwin, Giovanni Capasso, G GiebischAbstract:Potassium and sodium transport along the Loop of Henle: Effects of altered dietary potassium intake. We assessed the effects of changes in potassium (K + ) balance on the function of the Loop of Henle by a combination of renal clearance and microperfusion experiments. Rat superficial cortical nephrons were perfused in vivo at 20 nl · min -1 from late proximal to early distal tubule with an artificial end-proximal solution containing either 3.8 or 1.8 m M potassium. Rats were fed a control diet, a low-potassium diet for at least three weeks, or a high-potassium diet for 10 to 14 days. When compared with the appropriate end-proximal potassium concentration in the perfusion fluid, potassium absorption along the Loop of Henle (J K ) increased in potassium-depletion whereas sodium (J Na ) and fluid (J v ) absorption decreased. In rats fed a high-potassium diet, absorption of potassium, sodium and fluid was depressed. We propose that changes of external potassium balance affect the transport of electrolytes and fluid along the Loop of Henle in vivo by modulating the transport of potassium and sodium primarily in the thick ascending limb. Changes in potassium reabsorption may also be affected by alterations of potassium-recycling.
Robert J Unwin - One of the best experts on this subject based on the ideXlab platform.
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bicarbonate transport along the Loop of Henle molecular mechanisms and regulation
Journal of Nephrology, 2002Co-Authors: Giovambattista Capasso, Robert J Unwin, Maria Rosaria Rizzo, A Pica, G GiebischAbstract:The Loop of Henle (LOH) is an important site of renal tubule acidification. A combination of several techniques, including in vivo microperfusion, perfusion in vitro of the S3 segment of the proximal tubule and of the thick ascending limb (TAL) of Henle's Loop, as well as quantitative PCR performed on isolated TAL, has permitted the definition of key transporters and their role in modulating bicarbonate reabsorption in physiological and pathophysiological conditions. Na(+)-H+ exchange is the most important transport mechanism responsible for bicarbonate reabsorption, although a small but significant contribution of H(+)-ATPase-mediated bicarbonate reabsorption can also be identified. NHE3 is the main of several NHE isoforms expressed in the TAL and in the S3 segment of the proximal tubule. Special properties of the Na(+)-H+ exchanger in the TAL are its relative insensitivity to changes in cell pH (pHi) and the tight coupling between apical and basolateral Na(+)-H+ exchange. Several hormones, including anti-diuretic hormone (ADH), angiotensin II (AII), and gluco- and mineralocorticoids regulate Na(+)-H+ exchange. Loop diuretics such as furosemide stimulate bicarbonate transport along the LOH. Systemic acid-base disturbances also modulate bicarbonate transport: acidosis increases bicarbonate reabsorption, while metabolic alkalosis has the opposite effect. Neither hypokalemic alkalosis nor respiratory alkalosis or respiratory acidosis alter bicarbonate transport along the LOH. A significant role of HCO3 backflux, most likely through the paracellular pathway of the TAL, can also be observed. Changes in extracellular osmolality also affect bicarbonate reabsorption: hypertonicity inhibits, whereas hypotonicity stimulates transport. Transport activation is also observed as an adaptive response to glomerular hyperfiltration.
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effects of the potassium channel blocker barium on sodium and potassium transport in the rat Loop of Henle in vivo
Experimental Physiology, 2001Co-Authors: S J Walter, David G Shirley, E J Folkerd, Robert J UnwinAbstract:In vitro evidence suggests that the ‘recycling’ of K + ions through luminal K + channels in the thick ascending limb of the Loop of Henle (TALH) is essential for the normal operation of the luminal Na + –K + –2Cl _ co-transporter. In the present study these channels were investigated in vivo by perfusing superficial Loops of Henle in anaesthetised rats with and without the K + channel blocker barium. Using a standard perfusate, intraluminal barium (5 mmol l _1 ) reduced sodium reabsorption (JNa) from 1887 ± 50 to 1319 ± 53 pmol min _1 ( P< 0.001). When the experiment was repeated using a low-Na + perfusate, designed to inhibit reabsorption in the pars recta (the initial segment of the Loop of Henle), a similar reduction in JNa was observed (from 698 ± 47 to 149 ± 23 pmol min _1 , P< 0.001), strongly suggesting that the effect of barium is localised to the TALH. The magnitude of the reduction in JNa during blockade of K + channels confirms the importance of K + recycling in facilitating Na + reabsorption in the TALH in vivo. However, the reduction in JNa was not associated with a fall in the K + concentration of the fluid collected at the early distal tubule. When bumetanide, an inhibitor of the Na + –K + –2Cl _ co-transporter, was included in the low-Na + perfusate, net K + secretion was observed. Addition of barium to this perfusate reduced, but did not abolish, the secretion, suggesting that bumetanide-induced K + secretion results partly from paracellular transport. Experimental Physiology (2001) 86.4, 469–474.
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contribution of na h exchange to sodium reabsorption in the Loop of Henle a microperfusion study in rats
The Journal of Physiology, 1998Co-Authors: D G Shirley, Robert J Unwin, S J Walter, G GiebischAbstract:1The contribution of apical Na+-H+ exchange to sodium reabsorption in the thick ascending limb of the Loop of Henle (TALH) in vivo was examined in anaesthetized rats by perfusing Loops of Henle of superficial nephrons with solutions containing the Na+-H+ exchange inhibitor, ethyl isopropyl amiloride (EIPA). 2Using a standard perfusate, no statistically significant effect of EIPA on net sodium reabsorption (JNa) was detected. However, when sodium reabsorption in the pars recta of the proximal tubule was minimized by using a low-sodium perfusate, EIPA reduced JNa from 828 ± 41 to 726 ± 37 pmol min−1 (P < 0.05), indicating that apical Na+-H+ exchange can make a small contribution to net sodium reabsorption in the TALH in vivo. This contribution appears to be dependent on the bicarbonate load, since an increase in the latter led to an enhancement of EIPA-sensitive sodium transport. 3Addition of the Na+-K+-2Cl− cotransport inhibitor, bumetanide, to the low-sodium perfusate reduced baseline JNa to 86 ± 27 pmol min−1. In this setting, EIPA reduced JNa further, to −24 ± 18 pmol min−1 (P < 0.05), an effect similar to that seen in the absence of bumetanide. This finding argues against previous suggestions (based on in vitro evidence) that inhibition of the Na+-K+-2Cl− cotransporter leads to an increase in apical Na+-H+ exchange in the TALH.
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Contribution of Na+-H+ exchange to sodium reabsorption in the Loop of Henle: a microperfusion study in rats
The Journal of Physiology, 1998Co-Authors: D G Shirley, S J Walter, Robert J Unwin, Gerhard GiebischAbstract:1The contribution of apical Na+-H+ exchange to sodium reabsorption in the thick ascending limb of the Loop of Henle (TALH) in vivo was examined in anaesthetized rats by perfusing Loops of Henle of superficial nephrons with solutions containing the Na+-H+ exchange inhibitor, ethyl isopropyl amiloride (EIPA). 2Using a standard perfusate, no statistically significant effect of EIPA on net sodium reabsorption (JNa) was detected. However, when sodium reabsorption in the pars recta of the proximal tubule was minimized by using a low-sodium perfusate, EIPA reduced JNa from 828 ± 41 to 726 ± 37 pmol min−1 (P < 0.05), indicating that apical Na+-H+ exchange can make a small contribution to net sodium reabsorption in the TALH in vivo. This contribution appears to be dependent on the bicarbonate load, since an increase in the latter led to an enhancement of EIPA-sensitive sodium transport. 3Addition of the Na+-K+-2Cl− cotransport inhibitor, bumetanide, to the low-sodium perfusate reduced baseline JNa to 86 ± 27 pmol min−1. In this setting, EIPA reduced JNa further, to −24 ± 18 pmol min−1 (P < 0.05), an effect similar to that seen in the absence of bumetanide. This finding argues against previous suggestions (based on in vitro evidence) that inhibition of the Na+-K+-2Cl− cotransporter leads to an increase in apical Na+-H+ exchange in the TALH.
S J Walter - One of the best experts on this subject based on the ideXlab platform.
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effects of the potassium channel blocker barium on sodium and potassium transport in the rat Loop of Henle in vivo
Experimental Physiology, 2001Co-Authors: S J Walter, David G Shirley, E J Folkerd, Robert J UnwinAbstract:In vitro evidence suggests that the ‘recycling’ of K + ions through luminal K + channels in the thick ascending limb of the Loop of Henle (TALH) is essential for the normal operation of the luminal Na + –K + –2Cl _ co-transporter. In the present study these channels were investigated in vivo by perfusing superficial Loops of Henle in anaesthetised rats with and without the K + channel blocker barium. Using a standard perfusate, intraluminal barium (5 mmol l _1 ) reduced sodium reabsorption (JNa) from 1887 ± 50 to 1319 ± 53 pmol min _1 ( P< 0.001). When the experiment was repeated using a low-Na + perfusate, designed to inhibit reabsorption in the pars recta (the initial segment of the Loop of Henle), a similar reduction in JNa was observed (from 698 ± 47 to 149 ± 23 pmol min _1 , P< 0.001), strongly suggesting that the effect of barium is localised to the TALH. The magnitude of the reduction in JNa during blockade of K + channels confirms the importance of K + recycling in facilitating Na + reabsorption in the TALH in vivo. However, the reduction in JNa was not associated with a fall in the K + concentration of the fluid collected at the early distal tubule. When bumetanide, an inhibitor of the Na + –K + –2Cl _ co-transporter, was included in the low-Na + perfusate, net K + secretion was observed. Addition of barium to this perfusate reduced, but did not abolish, the secretion, suggesting that bumetanide-induced K + secretion results partly from paracellular transport. Experimental Physiology (2001) 86.4, 469–474.
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localization of diuretic effects along the Loop of Henle an in vivo microperfusion study in rats
Clinical Science, 2000Co-Authors: R Unwin, G Giebisch, Giovambattista Capasso, S J Walter, David G ShirleyAbstract:In order to clarify the effects on sodium reabsorption in the Loop of Henle of methazolamide (a carbonic anhydrase inhibitor), chlorothiazide and the Loop diuretics frusemide and bumetanide, superficial Loops were perfused in vivo in anaesthetized rats and the individual diuretics were included in the perfusate. Differentiation between effects in the pars recta and in the thick ascending limb of Henle (TALH) was achieved by comparing responses to the diuretics when using a standard perfusate, designed to mimic native late proximal tubular fluid, and a low-sodium perfusate, designed to block net sodium reabsorption in the pars recta. With the standard perfusate, methazolamide caused decreases in sodium reabsorption (J(Na)) and water reabsorption (J(V)); with the low-sodium perfusate, a modest effect on J(Na) persisted, suggesting that carbonic anhydrase inhibition reduces sodium reabsorption in both the pars recta and the TALH. The effects of chlorothiazide were very similar to those of methazolamide with both the standard and low-sodium perfusates, suggesting that chlorothiazide also inhibits sodium reabsorption in the pars recta and TALH, perhaps through inhibition of carbonic anhydrase. With the standard perfusate, both frusemide and bumetanide produced the expected large decreases in J(Na), but J(V) was also lowered. With the low-sodium perfusate, the inhibitory effects of the Loop diuretics, particularly those of frusemide, were substantially reduced, while net potassium secretion was found. These observations indicate that a significant component of the effect of frusemide (and possibly of bumetanide) on overall sodium reabsorption is located in the pars recta, and that Loop diuretics induce potassium secretion in the TALH.
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contribution of na h exchange to sodium reabsorption in the Loop of Henle a microperfusion study in rats
The Journal of Physiology, 1998Co-Authors: D G Shirley, Robert J Unwin, S J Walter, G GiebischAbstract:1The contribution of apical Na+-H+ exchange to sodium reabsorption in the thick ascending limb of the Loop of Henle (TALH) in vivo was examined in anaesthetized rats by perfusing Loops of Henle of superficial nephrons with solutions containing the Na+-H+ exchange inhibitor, ethyl isopropyl amiloride (EIPA). 2Using a standard perfusate, no statistically significant effect of EIPA on net sodium reabsorption (JNa) was detected. However, when sodium reabsorption in the pars recta of the proximal tubule was minimized by using a low-sodium perfusate, EIPA reduced JNa from 828 ± 41 to 726 ± 37 pmol min−1 (P < 0.05), indicating that apical Na+-H+ exchange can make a small contribution to net sodium reabsorption in the TALH in vivo. This contribution appears to be dependent on the bicarbonate load, since an increase in the latter led to an enhancement of EIPA-sensitive sodium transport. 3Addition of the Na+-K+-2Cl− cotransport inhibitor, bumetanide, to the low-sodium perfusate reduced baseline JNa to 86 ± 27 pmol min−1. In this setting, EIPA reduced JNa further, to −24 ± 18 pmol min−1 (P < 0.05), an effect similar to that seen in the absence of bumetanide. This finding argues against previous suggestions (based on in vitro evidence) that inhibition of the Na+-K+-2Cl− cotransporter leads to an increase in apical Na+-H+ exchange in the TALH.
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Contribution of Na+-H+ exchange to sodium reabsorption in the Loop of Henle: a microperfusion study in rats
The Journal of Physiology, 1998Co-Authors: D G Shirley, S J Walter, Robert J Unwin, Gerhard GiebischAbstract:1The contribution of apical Na+-H+ exchange to sodium reabsorption in the thick ascending limb of the Loop of Henle (TALH) in vivo was examined in anaesthetized rats by perfusing Loops of Henle of superficial nephrons with solutions containing the Na+-H+ exchange inhibitor, ethyl isopropyl amiloride (EIPA). 2Using a standard perfusate, no statistically significant effect of EIPA on net sodium reabsorption (JNa) was detected. However, when sodium reabsorption in the pars recta of the proximal tubule was minimized by using a low-sodium perfusate, EIPA reduced JNa from 828 ± 41 to 726 ± 37 pmol min−1 (P < 0.05), indicating that apical Na+-H+ exchange can make a small contribution to net sodium reabsorption in the TALH in vivo. This contribution appears to be dependent on the bicarbonate load, since an increase in the latter led to an enhancement of EIPA-sensitive sodium transport. 3Addition of the Na+-K+-2Cl− cotransport inhibitor, bumetanide, to the low-sodium perfusate reduced baseline JNa to 86 ± 27 pmol min−1. In this setting, EIPA reduced JNa further, to −24 ± 18 pmol min−1 (P < 0.05), an effect similar to that seen in the absence of bumetanide. This finding argues against previous suggestions (based on in vitro evidence) that inhibition of the Na+-K+-2Cl− cotransporter leads to an increase in apical Na+-H+ exchange in the TALH.
Richard J Roman - One of the best experts on this subject based on the ideXlab platform.
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effects of 20 hete on na transport and na k atpase activity in the thick ascending Loop of Henle
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2007Co-Authors: Bernardo Lopez, Elisabete Dos A Santos, John R Falck, Richard J RomanAbstract:Previous studies have indicated that 20-hydroxyeicosatetraenoic acid (20-HETE) inhibits Na+ transport in the medullary thick ascending Loop of Henle (mTALH), but the mechanisms involved remain unce...
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Effects of 20-HETE on Na+ transport and Na+ -K+ -ATPase activity in the thick ascending Loop of Henle.
American journal of physiology. Regulatory integrative and comparative physiology, 2007Co-Authors: Bernardo Lopez, John R Falck, Elisabete A. Dos Santos, Richard J RomanAbstract:Previous studies have indicated that 20-hydroxyeicosatetraenoic acid (20-HETE) inhibits Na+ transport in the medullary thick ascending Loop of Henle (mTALH), but the mechanisms involved remain unce...
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enhanced chloride reabsorption in the Loop of Henle in dahl salt sensitive rats
Hypertension, 1991Co-Authors: Richard J Roman, Mary L KaldunskiAbstract:This study examines the nephron segments contributing to the blunted pressure-natriuretic response in Dahl salt-sensitive rats. Urine and late proximal and early distal tubular fluid samples were collected from 16-20-week-old, inbred Dahl salt-sensitive (DS/Jr) and salt-resistant (DR/Jr) rats, and Dahl salt-sensitive (DS) and salt-resistant (DR) rats from the Brookhaven colony, that were maintained from birth on a low (0.3%) sodium chloride diet. Urine flow and sodium and chloride excretions were 65% less in the DS/Jr than in the DR/Jr rats when their kidneys were perfused at an equal renal perfusion pressure of approximately 150 mm Hg. The percentages of the filtered load of water and chloride remaining at the end of the proximal tubule were significantly greater in DS/Jr rats than in DR/Jr rats; however, the percentages of the filtered load of water and chloride reaching the early distal tubule were significantly less, by 29% and 77%, respectively. Fractional reabsorption of water and chloride in the Loop of Henle of DS/Jr rats was twice that observed in DR/Jr rats. Similar results were obtained in DS and DR rats of the Brookhaven strain. Urine flow and sodium and chloride excretions were 60% lower in DS than in DR rats at a renal perfusion pressure of 135 mm Hg. Proximal tubular reabsorption of water and chloride was similar in DS and DR rats; however, the percentages of the filtered load of water and chloride reabsorbed in the Loop of Henle were greater in DS than in DR rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Gary A. Quamme - One of the best experts on this subject based on the ideXlab platform.
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magnesium transport in the renal distal convoluted tubule
Physical Review, 2001Co-Authors: Long-jun Dai, Gordon Ritchie, Dirk Kerstan, Hyung Sub Kang, David E C Cole, Gary A. QuammeAbstract:The distal tubule reabsorbs ∼10% of the filtered Mg2+, but this is 70–80% of that delivered from the Loop of Henle. Because there is little Mg2+ reabsorption beyond the distal tubule, this segment ...
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glucagon and arginine vasopressin stimulate mg2 uptake in mouse distal convoluted tubule cells
American Journal of Physiology-renal Physiology, 1998Co-Authors: Long-jun Dai, Brian Bapty, Gordon Ritchie, Gary A. QuammeAbstract:Glucagon and arginine vasopressin (AVP) enhance renal magnesium conservation through actions within the Loop of Henle and the distal tubule. Studies were performed on an immortalized mouse distal c...
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Mechanisms of amiloride stimulation of Mg2+ uptake in immortalized mouse distal convoluted tubule cells
American Journal of Physiology-Renal Physiology, 1997Co-Authors: Long-jun Dai, Lynn A. Raymond, P. A. Friedman, Gary A. QuammeAbstract:The distal convoluted tubule reabsorbs approximately 10% of the filtered magnesium, which is approximately 70% of that delivered to it from the Loop of Henle. The cellular mechanisms of magnesium t...
