Effect of hypercalcemia on renal tubular handling of calcium and magnesium

1982 ◽  
Vol 60 (10) ◽  
pp. 1275-1280 ◽  
Author(s):  
Gary A. Quamme
Keyword(s):  
Urinary Excretion ◽  
Calcium Absorption ◽  
Sodium Absorption ◽  
Loop Of Henle ◽  
Magnesium Transport ◽  
Acute Elevation ◽  
Fractional Calcium Absorption ◽  
Calcium And Magnesium ◽  
Renal Tubular

Tubular calcium and magnesium transport was investigated in thyroparathyroidectomized rats following acute elevation of extracellular calcium concentration. Fractional urinary excretion of calcium increased from 0.2 to 8.3% and magnesium increased from 15 to 39%, while sodium increased modestly from 0.1 to 1.1%. Superficial proximal tubules, Henle's loop, and distal tubules were perfused in vivo to determine the segmental effects of hypercalcemia. Fractional calcium absorption within the loop of Henle was significantly less in the hypercalcemie rats (58%) compared with normal animals (86%). Magnesium transport was inhibited to a greater extent compared with calcium in the loop as the fractional reabsorption decreased from 78% in the normal rats to 35% in the hypercalcemie animals. Sodium absorption was inhibited by 8%. Absolute calcium and magnesium absorption within the superficial distal convoluted tubule increased about three- to four-fold with increased delivery to this segment. These data indicate that hypercalcemia inhibits calcium and magnesium transport relatively more than sodium absorption in the loop of Henle and that this action principally accounts for the increase in urinary excretion of these electrolytes.

Effects of Intraluminal sulfate on electrolyte transfers along the perfused rat nephron

1981 ◽  
Vol 59 (2) ◽  
pp. 122-130 ◽  
Author(s):  
Gary A. Quamme
Keyword(s):  
Proximal Tubule ◽  
Chloride Transport ◽  
Distal Tubule ◽  
Phosphate Transport ◽  
Loop Of Henle ◽  
Magnesium Transport ◽  
Calcium And Magnesium ◽  
A Site ◽  
Distal Delivery

Superficial nephrons were perfused in vivo to determine the effect of intraluminal sulfate (1–20 mM) on electrolyte reabsorption in the rat with special reference to calcium and magnesium transport. This technique allowed us the opportunity of investigating separate electrolyte transfers without alteration of extrarenal influences. The major amount of perfused sulfate was absorbed in the proximal tubule with little absorption distal to the late proximal collection site. Phosphate transport was not affected by high luminal sulfate concentrations indicating distinct reabsorptive mechanisms for these two anions. Intraluminal sulfate significantly inhibited calcium and magnesium reabsorption in the proximal tubule, loop of Henle, and superficial distal tubule, in distinction to modest effects on sodium transport in these nephron segments. Chloride transport was not altered. The inhibition of divalent cation transfer was not quantitively similar in the different tubule segments. Small amounts of sulfate completely inhibited proximal calcium and magnesium reabsorption with little effect on transport within the loop of Henle. Enhanced distal delivery of sulfate significantly inhibited calcium and magnesium reabsorption in the distal tubule, a site where the sulfate anion is not reabsorbed. These results demonstrate the importance of distal delivery of anionic ligands capable of forming nonreabsorbable complexes. Thus distal calcium and magnesium transport may be greatly modified by proximal control of anion reabsorption.

Effect of furosemide on calcium and magnesium transport in the rat nephron

1981 ◽  
Vol 241 (4) ◽  
pp. F340-F347 ◽  
Author(s):  
G. A. Quamme
Keyword(s):  
Ethacrynic Acid ◽  
Distal Tubule ◽  
Electrolyte Transport ◽  
Loop Of Henle ◽  
Transport Function ◽  
Magnesium Transport ◽  
Henle's Loop ◽  
Calcium And Magnesium ◽  
Single Tubules

Superficial tubules were perfused in vivo to determine the effect of intraluminal furosemide on electrolyte transport in the loop of Henle and distal tubule of the rat with special reference to calcium and magnesium reabsorption. in vivo perfusion of single tubules allowed us the opportunity to investigate separate electrolyte transfers with altering the corticomedullary concentration gradient within the kidney. Intraluminal furosemide (3 X 10(-6) and 3 X 10(-5) M) resulted in proportionately greater calcium and magnesium inhibition relative to sodium and chloride in Henle's loop. Furosemide had little effect on transport function within the perfused superficial distal tubule. Distal calcium and magnesium reabsorption was dependent on their respective deliveries to this segment. Parathyroid hormone increased fractional calcium and magnesium reabsorption in Henle's loop and the distal tubule in the presence of intraluminal furosemide. These results are consistent with a luminal effect of furosemide in the loop of Henle that inhibits calcium and magnesium transport to a greater degree than sodium chloride. Intraluminal ethacrynic acid (10(-4) M) or its cysteine complex had no effect on electrolyte transport in the perfused rat nephron.

Effect of calcitonin on calcium and magnesium transport in rat nephron

1980 ◽  
Vol 238 (6) ◽  
pp. E573-E578 ◽  
Author(s):  
G. A. Quamme
Keyword(s):  
Calcium Concentration ◽  
Transport Model ◽  
Distal Tubule ◽  
Urinary Calcium ◽  
Plasma Calcium ◽  
Loop Of Henle ◽  
Plasma Calcium Concentration ◽  
Calcium And Magnesium ◽  
Magnesium Excretion

Renal calcium and magnesium reabsorption was investigated in young, thyroparathyroidectomized rats receiving synthetic salmon calcitonin. Kidney and tubular function was assessed by clearance and in vivo microperfusion techniques, respectively. Calcitonin reduced urinary calcium and magnesium excretion that was attributed to increased reabsorption within the loop of Henle. This enchanced reabsorption was independent of parathyroid hormone; however, it is contingent on a decline in plasma calcium concentration. Prevention of hypocalcemia by CaCl2 infusion in rats acutely administered calcitonin resulted in loop function comparable to animals not receiving the hormone. Calcitonin had little effect on proximal tubule or distal tubule electrolyte reabsorption. These results are consistent with a transport model for calcium and magnesium in the loop of Henle involving a contraluminal transfer step modulated by absolute extracellular calcium or magnesium. Furthermore, these studies suggest that the discrepancies present in the literature concerning renal effects of calcitonin on electrolyte reabsorption are due to variations in observed hormone action, namely, the effect on plasma calcium concentration.

scholarly journals Renalase regulates peripheral and central dopaminergic activities

2015 ◽  
Vol 308 (2) ◽  
pp. F84-F91 ◽  
Author(s):  
Janete Quelhas-Santos ◽  
Maria Paula Serrão ◽  
Isabel Soares-Silva ◽  
Cátia Fernandes-Cerqueira ◽  
Liliana Simões-Silva ◽  
...  
Keyword(s):  
Amino Acid ◽  
Urinary Excretion ◽  
Plasma Levels ◽  
Amine Oxidase ◽  
Acid Decarboxylase ◽  
Wild Type ◽  
Amino Acid Decarboxylase ◽  
Renal Tubular ◽  
In Vivo Administration

Renalase is a recently identified FAD/NADH-dependent amine oxidase mainly expressed in kidney that is secreted into blood and urine where it was suggested to metabolize catecholamines. The present study evaluated central and peripheral dopaminergic activities in the renalase knockout (KO) mouse model and examined the changes induced by recombinant renalase (RR) administration on plasma and urine catecholamine levels. Compared with wild-type (WT) mice, KO mice presented increased plasma levels of epinephrine (Epi), norepinephrine (NE), and dopamine (DA) that were accompanied by increases in the urinary excretion of Epi, NE, DA. In addition, the KO mice presented an increase in urinary DA-to-l-3,4-dihydroxyphenylalanine (l-DOPA) ratios without changes in renal tubular aromatic-l-amino acid decarboxylase (AADC) activity. By contrast, the in vivo administration of RR (1.5 mg/kg sc) to KO mice was accompanied by significant decreases in plasma levels of Epi, DA, and l-DOPA as well as in urinary excretion of Epi, DA, and DA-to-l-DOPA ratios notwithstanding the accompanied increase in renal AADC activity. In addition, the increase in renal DA output observed in renalase KO mice was accompanied by an increase in the expression of the L-type amino acid transporter like (LAT) 1 that is reversed by the administration of RR in these animals. These results suggest that the overexpression of LAT1 in the renal cortex of the renalase KO mice might contribute to the enhanced l-DOPA availability/uptake and consequently to the activation of the renal dopaminergic system in the presence of renalase deficiency.

Calcium transport in the proximal convoluted tubule and loop of Henle of rats made diabetic with streptozotocin

1991 ◽  
Vol 131 (3) ◽  
pp. 373-380 ◽  
Author(s):  
H. O. Garland ◽  
P. J. Harris ◽  
T. O. Morgan
Keyword(s):  
Calcium Absorption ◽  
Diabetic Rats ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Fluid Absorption ◽  
New Information ◽  
Causative Factors ◽  
Nephron Segment ◽  
Acute Changes

ABSTRACT In-vivo microperfusion was used to localize the reabsorptive defect responsible for the hypercalciuria of diabetes mellitus and to investigate possible causative factors. Unidirectional proximal calcium absorption was not significantly different in rats made diabetic with streptozotocin compared with controls, providing evidence against the involvement of this nephron segment in the phenomenon. Calcium absorption by the loop of Henle, was however, significantly (P<0·01) lower in diabetic animals (32·1 ±1·2 vs 40·4±0·6 pmol/min). Based on our knowledge of calcium movements within the loop, it is likely that the reabsorptive defect resides within the thick ascending limb. The calcium lesion was found to be independent of acute changes in intraluminal glucose concentration and could not be corrected by acute insulin treatment. The study also provides new information on the relationship between intratubular glucose and fluid movements in the rat nephron. In diabetic rats a proximal perfusate containing 30 mmol glucose/l resulted in fluid absorption comparable with that seen in control rats perfused with 5 mmol glucose/l. However, intraluminal glucose had a stimulatory effect on fluid absorption in the loop of Henle of diabetic rats (10·7 ±0·5 vs 7·9±0·4 nl/min; P<0·01). Journal of Endocrinology (1991) 131, 373–380

Kinetic profile of overall elimination of 5-methyltetrahydropteroylglutamate in rats

1999 ◽  
Vol 276 (3) ◽  
pp. E580-E587 ◽  
Author(s):  
Yong-Hae Han ◽  
Yukio Kato ◽  
Hiroyuki Kusuhara ◽  
Hiroshi Suzuki ◽  
Minoru Shimoda ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
The Body ◽  
Parallel Increase ◽  
Liver Concentration ◽  
Renal Tubular Reabsorption ◽  
Total Body ◽  
Renal Tubular ◽  
Kinetics Of ◽  
Body Clearance

The in vivo biliary and urinary excretion kinetics of 5-methyltetrahydropteroylglutamate (5-CH3-H4PteGlu) were studied in rats. During infusion at various rates (48–965 nmol ⋅ h−1⋅ kg−1), the total body clearance (CLtotal) of 5-CH3-H4PteGlu could be attributed almost entirely to the sum of the biliary and urinary (CLurine,p) excretion clearances. After a 4-h infusion at the highest rate, the 5-CH3-H4PteGlu in the liver was 10 times higher than the endogenous level, whereas its polyglutamate form did not increase, suggesting that most of the infused 5-CH3-H4PteGlu is not incorporated in the polyglutamate pool but is eliminated by excretion. The parallel increase in CLtotaland CLurine,pwith the increase in infusion rate might result from saturation of reabsorption at the renal proximal tubules, since the urinary excretion clearance, defined with respect to the kidney concentration, also increased while the biliary excretion clearance, defined with respect to the liver concentration, remained almost constant. We conclude that the hepatobiliary excretion is a relatively low-affinity process with a constant clearance, whereas the renal tubular reabsorption is saturated at higher plasma 5-CH3-H4PteGlu concentration (∼0.5 μM). Urinary excretion becomes the predominant elimination route for any excess 5-CH3-H4PteGlu in the body.

ÉTUDES IN VIVO SUR LE MÉTABOLISME DES ANDROGÉNES APRES ADMINISTRATION DE STÉROÏDES INHIBITEURS DE L'OVULATION

1965 ◽  
Vol 50 (1) ◽  
pp. 131-144 ◽  
Author(s):  
P. Mauvais-Jarvis ◽  
M. F. Jayle ◽  
J. Decourt ◽  
J. Louchart ◽  
J. Truffert
Keyword(s):  
Luteinizing Hormone ◽  
Urinary Excretion ◽  
Normal Subjects ◽  
Hormone Activity ◽  
Testosterone Production ◽  
Normal Men ◽  
Ethinyl Oestradiol

ABSTRACT Normal subjects and hirsute women with micropolycystic ovaries were treated with ethinyl-oestrenol + 3-methoxy-ethinyl-oestradiol (Lyndiol®), in view of studying the action of this compound on the production of androgens and on the urinary excretion of their metabolites. In normal men, the production of testosterone and the excretion of androsterone and aetiocholanolone are suppressed, whereas the excretion of other 17-ketosteroids and the production of dehydroepiandrosterone sulphate are unchanged. Moreover, the luteinizing hormone activity (LH) in plasma is depressed. It seems that the preparation inhibits specifically the testicular androgen production, by suppressing the hypothalamo-hypophyseal control of LH. Testosterone production and urinary 17-ketosteroid excretion are modified in the same way in women with Stein-Leventhal's syndrome. Physiopathological and therapeutical implications which come from these results are discussed.

ATYPICAL ADRENAL HYPERFUNCTION: IN VIVO STUDIES AND INCUBATIONS OF ADRENAL TISSUE WITH 4-14C PROGESTERONE

1968 ◽  
Vol 58 (3_Suppl) ◽  
pp. S5-S34
Author(s):  
Joseph W. Goldzieher ◽  
Leonard R. Axelrod ◽  
Arthur S. Weissbein
Keyword(s):  
Urinary Excretion ◽  
Clinical Features ◽  
In Vivo Studies ◽  
Acth Stimulation ◽  
Adrenal Tissue ◽  
Adrenal Hyperfunction

ABSTRACT Six women with atypical forms of adrenal cortical hyperfunction were studied by means of urinary excretion of 17-ketosteroids and 17-hydroxycorticoids and their response to ACTH stimulation and corticosteroid suppression. Unusual responses were observed, particularly with respect to the independence of 17-KS and 17-OHCS excretion. The adrenals of 3 patients were anatomically normal whereas the others showed hyperplasia. Minced adrenal tissue was incubated with 4-14C progesterone and the metabolites isolated and definitively identified. The pattern of biosynthesized corticosteroids showed great variation, and in some instances clarified certain clinical features. The pattern of certain C19-metabolites could not be studied adequately because of the use of a Δ4 rather than a Δ5 substrate.

Effect of acid lumen pH on potassium transport in renal cortical collecting tubules

1976 ◽  
Vol 230 (1) ◽  
pp. 239-244 ◽  
Author(s):  
JF Boudry ◽  
LC Stoner ◽  
MB Burg
Keyword(s):  
Mean Value ◽  
Potassium Transport ◽  
Sodium Absorption ◽  
Positive Voltage ◽  
Tubule Lumen ◽  
Potassium Secretion ◽  
Transepithelial Voltage ◽  
Renal Tubular ◽  
Collecting Tubules

In order to determine the effect of acid lumen pH on renal tubular potassium transport, cortical collecting tubules were dissected from rabbit kidneys and perfused in vitro. When the pH of the perfusate was lowered from 7.4 to 6.8, potassium secretion into the tubule lumen decreased by an average of 47%. The transepithelial voltage increased from a mean value of -32 mV (lumen negative) at pH 7.4 to -51 mV at PH 6.8. Net sodium absorption from the tubule lumen was essentially unchanged (5% mean decrease). Transepithelial voltage and potassium secretion returned to control values when the pH of the perfusate was raised to 7.4. Alterations in pH of the bath had no comparable effect on the transepithelial voltage, whether the bath pH was increased or decreased. We conclude that a decrease in the pH of the tubule fluid of itself inhibits active potassium secretion in this tubule segment, providing an additional explanation for the decrease in potassium excretion found in acidosis. The negative voltage (presumably caused by sodium absorption out of the lumen) is increased under these conditions, possibly because of reduction of a smaller counterbalancing positive voltage caused by potassium secretion into the lumen.

Sign in / Sign up

Export Citation Format

Share Document