Effects of Low-dose Angiotensin II Infusion on Loop Segment Reabsorption: A Free-Flow Micropuncture Study in Rats

1995 ◽  
Vol 88 (3) ◽  
pp. 351-358 ◽  
Author(s):  
René Fransen ◽  
Walther H. Boer ◽  
Remmert De Roos ◽  
Peter Boer ◽  
Hein A. Koomans
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Low Dose ◽  
Distal Tubule ◽  
Fractional Excretion ◽  
Free Flow ◽  
Control Group ◽  
Aortic Constriction ◽  
Micropuncture Study ◽  
Reabsorption Rate

1. Little direct information is available on the actions of angiotensin II beyond the proximal tubule. We therefore studied the effect of a mildly vasoconstrictive dose of angiotensin II on tubular handling of water, sodium (Na+) and lithium (Li+) in rats by means of free-flow micropuncture at the late proximal tubule and the early distal tubule. 2. Endogenous angiotensin II was suppressed by pretreament with enalapril. Compared with a control group, angiotensin II increased mean arterial pressure by 15 mmHg. Glomerular filtration rate decreased from 1.32 ± 0.05 to 1.10 ± 0.05 ml/min, Na+ excretion from 0.43 ± 0.09 to 0.13 ± 0.03 μmol/min, fractional delivery of water at the late proximal tubule from 50.1 ± 1.7 to 42.9 ± 3.2%, fractional delivery of Na+ at the late proximal tubule from 46.5 ± 1.3 to 39.1 ± 3.5% and fractional delivery of water at the early distal tubule from 26.4 ± 1.4 to 21.9 ± 1.0% (P < 0.05 for each variable). Fractional delivery of Na+ at the early distal tubule did not change significantly. 3. Similar experiments were performed during partial aortic constriction to exclude the effects of increased perfusion pressure. The data obtained were similar, except that in this group the fractional delivery of Na+ at the early distal tubule decreased from 8.6 ± 0.7 to 6.8 ± 0.9% (P < 0.05). 4. The relation between late proximal tubule Na+ delivery and Na+ reabsorption between late proximal and early distal tubule was not disturbed by angiotensin II. For water, however, this relation tended to shift to a higher reabsorption rate. 5. The decrease in fractional excretion of Li+ followed the decrease in proximal reabsorption as measured directly by micropuncture. Angiotensin II infusion did not appear to affect Li+ reabsorption beyond the proximal tubule. Distal fractional Na+ reabsorption estimated by the Li+ clearance increased significantly during angiotensin II infusion. 6. In conclusion, our data indicate that a Na+-retaining dose of angiotensin II increases Na+ reabsorption in the proximal tubule, an effect correctly indicated by the change in the fractional excretion of Li+, does not influence Na+ reabsorption in the loop of Henle beyond the proximal tubule, but may increase Na+ reabsorption in more distal segments.

Inhibition of urate excretion by pyrazinoate: a micropuncture study

1975 ◽  
Vol 229 (6) ◽  
pp. 1604-1608 ◽  
Author(s):  
F Roch-Ramel ◽  
IM Weiner
Keyword(s):  
Proximal Tubule ◽  
Renal Clearance ◽  
Left Kidney ◽  
Distal Tubule ◽  
Major Effect ◽  
The Other ◽  
Free Flow ◽  
Clearance Ratio ◽  
Cebus Albifrons ◽  
Micropuncture Study

Anesthetized monkeys (Cebus albifrons) undergoing moderate mannitol diuresis were treated with infusions containing lithium urate to elevate the urate concentration in plasma to 45-68 mug/ml and containing the uricosuric drug, 2-nitroprobenecid, to enhance the renal clearance or urate. The urate/inulin clearance ratio was 0.55 +/- 0.03. When pyrazinoate was added to the infusion the clearance ratio fell to 0.26 +/- 0.02. Analysis of free-flow micropuncture samples revealed a major effect of pyrazinoate in the proximal tubule, although an additional, smaller action in the distal tubule could not be definitely excluded. When droplets containing [14C]urate and [3H]inulin were streaked on the surface of the left kidney more urate than inulin appeared in the urine from that kidney (but not the other) within the first 3 min after application. This "excess" excretion of urate could be largely eliminated by pretreatment with pyrazinoate. The results suggest that pyrazinoate inhibits secretion of urate in the proximal tubule.

Electrolyte handling by the superficial nephron of the rabbit

1986 ◽  
Vol 250 (4) ◽  
pp. F590-F595 ◽  
Author(s):  
N. L. Wong ◽  
S. J. Whiting ◽  
C. L. Mizgala ◽  
G. A. Quamme
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Concentration Ratio ◽  
Filtration Rate ◽  
Distal Tubule ◽  
Mean Value ◽  
Loop Of Henle ◽  
Collection Site ◽  
Micropuncture Study ◽  
The Mean

A micropuncture study of the rabbit was performed to evaluate the function of the superficial nephron. The mean glomerular filtration rate of the left micropunctured kidney was 4.0 +/- 0.8 ml/min. The concentration profile of electrolytes within the proximal tubule was similar to that of species previously investigated except for potassium. The mean tubular fluid (TF)-ultrafilterable (UF) concentration ratios were as follows: sodium, 1.01 +/- 0.03; chloride, 1.14 +/- 0.04; calcium, 1.12 +/- 0.04; magnesium, 1.47 +/- 0.08; and phosphate, 0.94 +/- 0.09, with a mean TF-plasma (P) inulin concentration ratio of 1.78 +/- 0.14 (n = 32). The TF/UF potassium value significantly increased in association with TF/P inulin to a mean value of 1.26 +/- 0.06. Accordingly, 29% of the filtered potassium was reabsorbed in the superficial proximal tubule compared with 43% of the filtered sodium. The loop of Henle reabsorbed 55-60% of the filtered sodium, chloride, and calcium, whereas considerably less magnesium (33%) was reabsorbed. Segments beyond the distal tubule collection site reabsorbed little of the delivered magnesium, which supports the notion that the loop of Henle is the principal segment accounting for adjustments in magnesium balance. These studies indicate that the superficial nephron of the rabbit performs similar to other species reported, except potassium reabsorption is significantly less in the proximal convoluted tubule.

Abstract P041: Proximal Tubule-specific Deletion Of Angiotensin Ii Type 1a Receptors In The Kidney Lowers Basal Blood Pressure And Attenuates Angiotensin Ii-induced Hypertension By Increasing Glomerular Filtration And The Pressure-natriuresis Response

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Xiao C Li ◽  
Ana P Leite ◽  
Liang Zhang ◽  
Jia L Zhuo
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Pressor Response ◽  
Control Group ◽  
Ang Ii ◽  
Induced Hypertension ◽  
Basal Blood Pressure ◽  
Pressure Natriuresis ◽  
Specific Deletion

The present study tested the hypothesis that intratubular angiotensin II (Ang II) and AT 1a receptors in the proximal tubules of the kidney plays an important role in basal blood pressure control and in the development of Ang II-induced hypertension. Mutant mice with proximal tubule-specific deletion of AT 1a receptors in the kidney, PT- Agtr1a -/- , were generated to test the hypothesis. Eight groups (n=7-12 per group) of adult male wild-type (WT) and PT- Agtr1a -/- mice were infused with or without Ang II for 2 weeks (1.5 mg/kg, i.p.). Basal systolic, diastolic, and mean arterial pressures were ~13 ± 3 mmHg lower in PT- Agtr1a -/- than WT mice ( P <0.01). Basal glomerular filtration rate (GFR), as measured using transdermal FITC-sinistrin, was significantly higher in PT- Agtr1a -/- mice (WT: 160.4 ± 7.0 μl/min vs. PT- Agtr1a -/- : 186.0 ± 6.0 μl/min, P <0.05). Basal 24 h urinary Na + excretion (U Na V) was significantly higher in PT- Agtr1a -/- than WT mice ( P <0.01). In response to Ang II infusion, both WT and PT- Agtr1a -/- mice developed hypertension, and the magnitude of the pressor response to Ang II was similar in WT (Δ43 ± 3 mmHg, P <0.01) and PT- Agtr1a -/- mice (Δ39 ± 5 mmHg, P <0.01). However, the absolute blood pressure level was still 16 ± 3 mmHg lower in PT- Agtr1a -/- mice ( P <0.01). Ang II significantly decreased GFR to 132.2 ± 7.0 μl/min in WT mice ( P <0.01), and to 129.4 ± 18.6 μl/min in PT- Agtr1a -/- mice ( P <0.01), respectively. In WT mice, U Na V increased from 139.3 ± 22.3 μmol/24 h in the control group to 196.4 ± 29.6 μmol/24 h in the Ang II-infused group ( P <0.01). In PT- Agtr1a -/- mice, U Na V increased from 172.0 ± 10.2 μmol/24 h in the control group to 264.7 ± 35.4 μmol/24 h in the Ang II-infused group ( P <0.01). The pressor response to Ang II was attenuated, while the natriuretic response was augmented by losartan in WT and PT- Agtr1a -/- mice ( P <0.01). Finally, proximal tubule-specific deletion of AT 1a receptors significantly augmented the pressure-natriuresis response and natriuretic responses to acute saline infusion ( P <0.01) or a 2% high salt diet ( P <0.01). We concluded that deletion of AT 1a receptors selectively in the proximal tubules lowers basal blood pressure and attenuates Ang II-induced hypertension by increasing GFR and promoting the natriuretic response in PT- Agtr1a -/- mice.

Micropuncture study of the superficial nephron of Perognathus penicillatus

1981 ◽  
Vol 241 (6) ◽  
pp. F612-F617
Author(s):  
E. J. Braun ◽  
D. R. Roy ◽  
R. L. Jamison
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Distal Tubule ◽  
Urine Osmolality ◽  
Small Rodent ◽  
Micropuncture Study ◽  
Single Nephron ◽  
Average Body

A micropuncture study of Perognathus penicillatus, a small rodent native to the deserts of the southwestern United States was performed to evaluate the function of the superficial nephron. Data are reported for 12 animals of 17 g average body wt. Mean glomerular filtration rate was 475 +/- 73 microliter X min-1 X g kidney wt-1. Urine osmolality averaged 1,154 +/- 197 mosmol/kg H2O. Single nephron glomerular filtration rate averaged 43 nl X min-1 X g kidney wt-1 in the proximal tubule and 48 in the distal tubule, values that are not significantly different. In terms of the filtered load remaining unreabsorbed at the end of the accessible proximal tubule, the average percentages were 46 water, 48 total solute, 45 sodium, 56 phosphorus, 62 potassium, 71 magnesium, and 54 calcium. The concentrations of potassium and magnesium in fluid samples increased significantly along the proximal tubule. Approximately at the midpoint of the distal tubule, fractional delivery of water, 13.1%, was greater than that for total solute, 10%, or sodium, 7%, indicating that the intervening segment of nephron reabsorbed solute and sodium in excess of water. The function of the superficial nephron resembles that of species previously investigated except for potassium reabsorption in the proximal convoluted tubule.

scholarly journals Dietary fructose enhances angiotensin II-stimulated Na+ transport via activation of PKC-α in renal proximal tubules

2020 ◽  
Vol 318 (6) ◽  
pp. F1513-F1519
Author(s):  
Nianxin Yang ◽  
Nancy J. Hong ◽  
Jeffrey L. Garvin
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Tap Water ◽  
Renal Proximal Tubule ◽  
Proximal Tubules ◽  
Control Group ◽  
Ang Ii ◽  
Dietary Fructose ◽  
Intracellular Ca ◽  
Pkc Β

Angiotensin II (ANG II) stimulates proximal nephron transport via activation of classical protein kinase C (PKC) isoforms. Acute fructose treatment stimulates PKC and dietary fructose enhances ANG II’s ability to stimulate Na+ transport, but the mechanisms are unclear. We hypothesized that dietary fructose enhances ANG II’s ability to stimulate renal proximal tubule Na+ reabsorption by augmenting PKC-α activation and increases in intracellular Ca2+. We measured total and isoform-specific PKC activity, basal and ANG II-stimulated oxygen consumption, a surrogate of Na+ reabsorption, and intracellular Ca2+ in proximal tubules from rats given either 20% fructose in their drinking water (fructose group) or tap water (control group). Total PKC activity was measured by ELISA. PKC-α, PKC-β, and PKC-γ activities were assessed by measuring particulate-to-soluble ratios. Intracelluar Ca2+ was measured using fura 2. ANG II stimulated total PKC activity by 53 ± 15% in the fructose group but not in the control group (−15 ± 11%, P < 0.002). ANG II stimulated PKC-α by 0.134 ± 0.026 but not in the control group (−0.002 ± 0.020, P < 0.002). ANG II increased PKC-γ activity by 0.008 ± 0.003 in the fructose group but not in the control group ( P < 0.046). ANG II did not stimulate PKC-β in either group. ANG II increased Na+ transport by 454 ± 87 nmol·min−1·mg protein−1 in fructose group, and the PKC-α/β inhibitor Gö6976 blocked this increase (−96 ± 205 nmol·min−1·mg protein−1, P < 0.045). ANG II increased intracellular Ca2+ by 148 ± 53 nM in the fructose group but only by 43 ± 10 nM in the control group ( P < 0.035). The intracellular Ca2+ chelator BAPTA blocked the ANG II-induced increase in Na+ transport in the fructose group. We concluded that dietary fructose enhances ANG II’s ability to stimulate renal proximal tubule Na+ reabsorption by augmenting PKC-α activation via elevated increases in intacellular Ca2+.

Tubular Handling of Phosphate along the Nephron of Thyroparathyroidectomized Rats Injected with Ethane-1-Hydroxy-1,1-Diphosphonate

1981 ◽  
Vol 60 (2) ◽  
pp. 171-177 ◽  
Author(s):  
R. C. Mühlbauer ◽  
J.-P. Bonjour ◽  
H. Fleisch
Keyword(s):  
Proximal Tubule ◽  
Bone Mineral ◽  
Adaptive Response ◽  
Distal Tubule ◽  
Tubular Reabsorption ◽  
Free Flow ◽  
Induced Changes ◽  
Terminal Nephron ◽  
Early Proximal Tubule

1. Previous studies have shown that in thyroparathyroidectomized rats injection of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) at doses that inhibit bone mineral retention (0.16 mmol = 10 mg of phosphorus/kg body wt. per day subcutaneously) leads to a decrease in the net tubular reabsorption of phosphate. 2. In the present work the tubular response to EHDP (0.16 mmol/kg body wt.) injected subcutaneously for 9 days has been localized by free-flow micropuncture in thyroparathyroidectomized rats. 3. The results show that the net tubular reabsorption of phosphate along the first portion of the (early) proximal tubule was markedly depressed in the EHDP-injected thyroparathyroidectomized rats compared with that in the pair-fed thyroparathyroidectomized control animals. In this latter group the delivery of phosphate to the distal tubule was larger than in the final urine, confirming previous reports. In the EHDP-injected thyroparathyroidectomized rats no difference in delivery of phosphate was found between the distal tubule and the final urine, suggesting that diphosphonate inhibited net reabsorption of phosphate in the terminal nephron. 4. The sites of the EHDP-induced changes in the tubular handling of phosphate were similar to those previously determined for the adaptive response to an increase in the supply of phosphate.

scholarly journals Low dose ouabain stimulates Na K ATPase α1 subunit association with angiotensin II type 1 receptor in renal proximal tubule cells

2016 ◽  
Vol 1863 (11) ◽  
pp. 2624-2636 ◽  
Author(s):  
Corey J. Ketchem ◽  
Clayton D. Conner ◽  
Rebecca D. Murray ◽  
Madalyn DuPlessis ◽  
Eleanor D. Lederer ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Low Dose ◽  
Renal Proximal Tubule ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Renal Proximal Tubule Cells ◽  
Α1 Subunit

scholarly journals Effect of propranolol on phosphate reabsorption by superficial nephron segments in response to parathyroid hormone in phosphate-deprived rats.

1990 ◽  
Vol 1 (2) ◽  
pp. 200-204
Author(s):  
A Rybczynska ◽  
A Hoppe ◽  
F G Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Free Flow ◽  
Phosphate Deprivation ◽  
Phosphate Reabsorption ◽  
Nephron Segments ◽  
Pars Recta

Phosphate deprivation causes a resistance to the phosphaturic effect of parathyroid hormone. The decreased phosphaturic response to parathyroid hormone in rats fed a low phosphate diet for 1 day can be restored by propranolol infusion. Free-flow micropuncture studies were performed to localize the nephron site of restoration of the phosphaturic effect of parathyroid hormone by propranolol in rats deprived of phosphate for one day. In animals fed low phosphate diet and in the presence of parathyroid hormone, propranolol infusion did not change phosphate delivery to the late proximal tubule; however, fractional delivery of phosphate to the early distal tubule was significantly increased from 18.3 +/- 2.9 to 32.2 +/- 4.1%. In rats fed a normal phosphate diet, propranolol infusion did not change phosphate delivery along the nephron. We conclude that the restoration of the phosphaturic effect of parathyroid hormone by propranolol infusion in rats deprived of phosphate for 1 day is primarily due to decreased reabsorption of phosphate by superficial loop segments, most likely the pars recta segment of the proximal tubule.

Nephron sites of action of nicotinamide on phosphate reabsorption

1984 ◽  
Vol 246 (1) ◽  
pp. F27-F31
Author(s):  
J. A. Haas ◽  
T. J. Berndt ◽  
A. Haramati ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Distal Tubule ◽  
Proximal Convoluted Tubule ◽  
Free Flow ◽  
Loop Of Henle ◽  
Phosphate Deprivation ◽  
Phosphate Reabsorption ◽  
Pars Recta ◽  
Sites Of Action

The administration of nicotinamide results in urinary phosphate excretions similar to those obtained with pharmacologic doses of parathyroid hormone (PTH). Free-flow micropuncture was performed to localize the nephron site(s) of inhibition of phosphate reabsorption by nicotinamide or PTH in thyroparathyroidectomized (TPTX) rats stabilized on a normal or low phosphate diet. In rats fed a normal phosphate diet phosphaturia was observed following either nicotinamide or PTH treatment. Nicotinamide inhibited phosphate reabsorption in the loop of Henle (pars recta) but not in the accessible proximal tubule. PTH inhibited phosphate reabsorption in both the accessible proximal tubule and the pars recta. In phosphate deprivation, the phosphaturic response to either nicotinamide or PTH was blunted. Although phosphate reabsorption was markedly inhibited in the accessible proximal tubule with both nicotinamide and PTH, subsequent reabsorption in the loop of Henle and distal tubule blunted the phosphaturia. We conclude that nicotinamide primarily inhibits phosphate reabsorption by the pars recta in rats fed a normal phosphate diet, whereas it inhibits phosphate reabsorption by the proximal convoluted tubule in rats fed a low phosphate diet. Furthermore, avid reabsorption of phosphate in the pars recta accounts for the resistance to the phosphaturic effect of nicotinamide or PTH seen in rats fed a low phosphate diet.

Renal filtration, reabsorption and excretion of aluminium in the rat

1992 ◽  
Vol 82 (1) ◽  
pp. 13-18 ◽  
Author(s):  
C. J. Lote ◽  
J. A. Wood ◽  
H. C. Saunders
Keyword(s):  
Plasma Concentration ◽  
Protein Binding ◽  
Low Dose ◽  
Fractional Excretion ◽  
Aluminium Chloride ◽  
Control Group ◽  
High Dose ◽  
High Concentration ◽  
Aluminium Concentration ◽  
The Difference

1. Plasma and urinary aluminium levels, and renal function, were investigated in a control group of rats (n = 5) and in two groups that received an intravenous bolus dose of aluminium chloride (either 25 μg or 800 μg of aluminium, n = 7 and 5, respectively). 2. In the control group (plasma aluminium concentration 76.8 ± 14.2 ng/ml), 59.4 ± 3.5% of the plasma aluminium was ultrafilterable. The percentage ultrafilterable after the administration of 25 μg of aluminium was 41.9 ± 7.8 (plasma concentration 154.3 ± 18.6 ng/ml). However, after administration of 800 μg of aluminium, to give a plasma concentration of 19800 ± 2956 ng/ml, only 1.06 ± 0.13% was ultrafilterable. 3. Such results have generally been interpreted as indicating an increase in protein-binding of aluminium with increasing aluminium concentration. In buffered aqueous solutions of aluminium chloride at pH 7.4, with an aluminium concentration of 189 ± 6 ng/ml, 96.12 ± 0.02% was ultrafilterable (n = 6). This concentration is comparable with that attained in the low-dose (25 μg) aluminium group of animals and suggests that the difference between the ultrafilterable percentage of aluminium in plasma compared with that in aqueous solution is indeed due to the binding of aluminium to high Mr material (proteins). In contrast, however, in an aqueous buffered (pH 7.4) solution containing 28200 ng of aluminium/ml, only 1.05 ± 0.09% was ultrafilterable. This indicates insolubility (i.e. colloid formation) of the aluminium at this high concentration. The same percentage (1.06 ± 0.13) was ultrafilterable from plasma from the high-dose (800 μg) aluminium group with a plasma aluminium concentration of 19 800 ± 2956 ng/ ml. This low ultrafilterable fraction is thus attributable to the insolubility of aluminium at this concentration, rather than to protein binding. 4. The fractional excretion of aluminium in the control group was approximately 10%. It was somewhat higher in the low-dose aluminium group, and reached 53% in the high-dose aluminium group. Nevertheless, it is clear that the kidneys are inefficient at excreting aluminium, so that after aluminium administration there is a prolonged period (several hours) during which the plasma aluminium concentration remains elevated and thus tissue deposition may occur.

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