Proximal tubular function in transgenic mice overexpressing atrial natriuretic factor

1994 ◽  
Vol 72 (10) ◽  
pp. 1168-1170 ◽  
Author(s):  
H. Sonnenberg ◽  
U. Honrath ◽  
C. K. Chong ◽  
L. J. Field ◽  
A. T. Veress
Keyword(s):  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Tubular Function ◽  
Nephron Filtration Rate ◽  
Natriuretic Factor ◽  
Single Nephron Filtration Rate ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Proximal Tubular Function ◽  
Atrial Natriuretic

A transgenic mouse model in which atrial natriuretic factor (ANF) expression is targeted to the liver was used to study intrarenal adjustments to the chronically elevated hormone level. Such animals, designated TTR-ANF, are characterized by reduced arterial blood pressure but similar sodium excretion compared with nontransgenic siblings. Proximal tubular micro-puncture gave the following results: single-nephron filtration rate = 12.7 ± 1.1 vs. 15.6 ± 1.9 nL/min (TTR-ANF versus nontransgenic, ns); end-proximal tubular fluid/plasma concentration ratio of inulin = 1.93 ± 0.09 vs. 1.97 ± 0.15 (ns); fractional reabsorption of sodium = 45.5 ± 2.8 vs. 46.0 ± 3.8% (ns); fractional reabsorption of chloride = 33.6 ± 3.3 vs. 32.4 ± 4.1% (ns). These data indicate that life-long elevation of plasma ANF concentration was not associated with significant alteration in single-nephron filtration rate and proximal tubular function. We conclude that compensatory anti-natriuretic mechanisms, localized downstream from the proximal tubule, can prevent ANF natriuresis.Key words: micropuncture, single-nephron filtration rate, sodium chloride reabsorption.

Measurement of nephron filtration in the dog: role of proximal intratubular pressure

1981 ◽  
Vol 241 (3) ◽  
pp. F238-F243
Author(s):  
D. A. Hartupee ◽  
A. H. Gillies ◽  
F. G. Knox
Keyword(s):  
Proximal Tubule ◽  
Filtration Rate ◽  
Free Flow ◽  
Nephron Filtration Rate ◽  
Intratubular Pressure ◽  
Single Nephron Filtration Rate ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Pressure Controlled

Previous studies concerning the measurement of single nephron filtration rate have shown that collections of proximal tubular fluid, in which an oil drop is held in a constant position, do not affect intratubular pressure in the early proximal tubule in the hydropenic rat. Since intratubular pressures are higher in the dog than the rat, we investigated the effect of position-controlled collections on proximal pressure and single nephron filtration rate (SNGFR) in the dog. During position-controlled collections, early proximal pressure fell 5.8 +/- 0.9 mmHg and SNGFR was 76.3 +/- 5.3 nl/min. During proximal re-collections, in which proximal pressure was maintained near the free-flow value using a long immobile oil block, SNGFR was significantly less, 44.4 +/- 5.5 nl/min. For each micropunctured kidney, SNGFR was also estimated by dividing GFR by the number of glomeruli (mean, 5.4 +/- 0.5 X 10(5)). Estimated SNGFR (50.9 +/- 6.3 nl/min) was not significantly different from pressure-controlled SNGFR but was significantly less than position-controlled SNGFR. Accordingly, in the dog, early proximal pressure decreases during position-controlled collection of proximal tubular fluid, resulting in an overestimation of SNGFR. This artifact can be avoided by controlling the intratubular pressure during collection of tubular fluid.

Atrial natriuretic factor can increase renal solute excretion primarily by raising glomerular filtration

1986 ◽  
Vol 250 (4) ◽  
pp. F710-F714 ◽  
Author(s):  
M. G. Cogan
Keyword(s):  
Glomerular Filtration ◽  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Control Level ◽  
Aortic Constriction ◽  
Natriuretic Factor ◽  
Tubular Transport ◽  
Single Nephron ◽  
Solute Excretion ◽  
Atrial Natriuretic

Controversy persists on whether atrial natriuretic factor (ANF) raises renal solute excretion simply by increasing glomerular filtration rate (GFR) or whether it directly inhibits tubular transport (independent of changes in flow rate). Free-flow micropuncture techniques were used in 10 Munich-Wistar rats. ANF caused a significant increase in single-nephron and whole-kidney GFR (41.6 +/- 1.4 to 52.7 +/- 2.3 nl/min and 0.95 +/- 0.05 to 1.24 +/- 0.09 ml/min, respectively). Although absolute proximal sodium, bicarbonate, and chloride reabsorption increased, the increment in reabsorption was less than the increase in load; therefore solute delivery out of the proximal tubule increased by approximately 30-35%. Whole-kidney electrolyte excretion also rose markedly. When single-nephron and whole-kidney GFR were reduced back to a control level by aortic constriction (40.2 +/- 1.8 nl/min and 0.93 +/- 0.05 ml/min, respectively), proximal transport reverted to normal values despite persistent ANF administration. Ninety percent of the ANF-induced natriuresis and chloruresis were simultaneously abolished when GFR was normalized. In conclusion, ANF has no direct effect on reabsorption in the superficial proximal convoluted tubule independent of changes in filtration rate. Although direct effects on more distal or deeper nephron segments are not precluded, the present data suggest that ANF can increase renal solute excretion predominantly by acutely augmenting GFR.

The Renal Response to Blood Volume Expansion in the Rat: Proximal Tubular Function and Urinary Excretion

1971 ◽  
Vol 49 (6) ◽  
pp. 525-535 ◽  
Author(s):  
H. Sonnenberg
Keyword(s):  
Blood Volume ◽  
Filtration Rate ◽  
Renal Excretion ◽  
Tubular Function ◽  
Volume Increase ◽  
Blood Volume Expansion ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Proximal Tubular Function ◽  
Proximal Convolution

Chronically salt- and deoxycorticosterone-acetate-loaded (DOCA) rats and chronically salt-deficient (NaD) rats were infused with blood, and consequent changes in renal excretion of water and electrolytes were compared with simultaneous alterations in proximal tubular function. During the period of intravascular expansion maintained by reinfusion of urine, diuresis and natriuresis, significant compared to control excretion, were seen in both groups. Although absolute levels of diuresis were not statistically different, DOCA rats excreted more sodium and less potassium than NaD rats; total cation excretion (Na+K) was comparable. A 10% reduction in proximal fractional reabsorption occurred in both series, associated, however, with large similar increases in single nephron filtration rate, so that absolute rates of proximal fluid reabsorption were actually increased. No correlation was found between changes in fractional or absolute reabsorption and renal excretion. Since vascular expansion results in similar alterations of filtration rate and proximal transport in both groups, the different ratios of excretion of sodium and potassium must be due to differences in tubular function at sites distal to the proximal convolution. The lack of direct correlation between proximal function and magnitude of renal excretion in these experiments further suggests that the excretory response to blood volume increase is determined ultimately by tubular mechanisms located in the distal part of the nephron.

Atrial Natriuretic Factor and Angiotensin Ii Stimulate Nitric Oxide Release from Human Proximal Tubular Cells

1995 ◽  
Vol 89 (5) ◽  
pp. 527-531 ◽  
Author(s):  
J. S. McLay ◽  
P. K. Chatterjee ◽  
S. K. Mistry ◽  
R. P. Weerakody ◽  
A. G. Jardine ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Nitric Oxide Production ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Oxide Production ◽  
Natriuretic Factor ◽  
Proximal Tubular ◽  
Atrial Natriuretic

1. It has been recently reported that angiotensin II can enhance atrial natriuretic factor-stimulated cyclic GMP release from brain capillary endothelial cells and stimulate directly the release of cyclic GMP by Neuro 2a cells. A possible mechanism mediating such cyclic GMP release could be via the production of nitric oxide and the resultant stimulation of soluble guanylate cyclase. 2. The ability of angiotensin II, atrial natriuretic factor and c(4–23) atrial natriuretic factor to stimulate nitric oxide production was investigated in primary cultures of human proximal tubular cells. 3. Freshly prepared human proximal tubular cells were seeded onto 6-well plates and allowed to reach confluence. Cells were then incubated with incremental concentrations of either angiotensin II, atrial natriuretic factor or c(4–23) atrial natriuretic factor alone for 1, 4, 12 or 24 h or in the presence of the nitric oxide synthase inhibitor NG-monomethyl-l-arginine. Angiotensin II was also incubated with human proximal tubular cells in the presence of the AT, and AT2 receptor antagonists DuP 753 and PD 123319. 4. Incubation of human proximal tubular cells with angiotensin II, atrial natriuretic factor or c(4–23) atrial natriuretic factor produced a dose- and time-dependent increase in nitric oxide production, which was inhibited in the presence of NG-monomethyl-l-arginine. A similar increase in nitric oxide production was observed after incubation with atrial natriuretic factor or c(4–23) atrial natriuretic factor. 5. The angiotensin-induced increase in nitric oxide production was not inhibited in the presence of either the angiotensin AT1 or AT2 receptor antagonists DuP 753 or PD 123319. 6. This study demonstrates that primary cultures of human proximal tubular cells can be stimulated to produce nitric oxide by both atrial natriuretic factor and angiotensin II. Furthermore, the atrial natriuretic factor-induced response appears to be mediated via the atrial natriuretic factor-C receptor, while the angiotensin II-induced response appears to be mediated by a novel, as yet unidentified, angiotensin II receptor.

Measurement of Single Nephron Filtration Rate in the Kidney of the River Lamprey, Lampetra Fluviatilis L

1978 ◽  
Vol 77 (1) ◽  
pp. 57-69 ◽  
Author(s):  
R. J. MORIARTY ◽  
A. G. LOGAN ◽  
J. C. RANKIN
Keyword(s):  
Filtration Rate ◽  
Gel Filtration ◽  
Reference Substance ◽  
Nephron Filtration Rate ◽  
River Lamprey ◽  
Peritubular Capillaries ◽  
Single Nephron Filtration Rate ◽  
Single Nephron ◽  
51Cr Edta ◽  
Renal Clearances

The reliability of [3H]inulin as a reference substance for the measurement of glomerular filtration rate (GFR) in river lampreys was investigated. Simultaneously measured renal clearances of [3H]inulin and [14C]-polyethylene glycol (PEG) were not significantly different. Recoveries of [3H]inulin in the urine following its injection into the proximal tubule and urinary duct averaged 83.5±4.0% (n = 14) and 93.0±4.6% (n = 9) respectively. No evidence was obtained to suggest penetration of the tubular wall by [3H]inulin following its introduction into peritubular capillaries. Gel-filtration of lamprey plasma and urine produced no signs of any significant degradation of the inulin to fructose. [3H]inulin recoveries, though significantly below 100% (P < 0.001), were considered adequate to justify its use after allowing for possible sources of error. A mean single nephron filtration rate (SNGFR) value of 7.02±0.27 nl/min (n = 89) was obtained from the kidneys of anaesthetized freshwater lampreys. [51Cr]EDTA was found to be totally unsuitable for the measurement of GFR in this species.

Atrial natriuretic factor increases after a protein meal in man

1988 ◽  
Vol 75 (5) ◽  
pp. 495-498 ◽  
Author(s):  
Bernardo Rodríguez-Iturbe ◽  
José Herrera ◽  
Jolanta Gutkowska ◽  
Gustavo Parra ◽  
Jesús Coello
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
High Dose ◽  
Protein Meal ◽  
Natriuretic Factor ◽  
Meat Meal ◽  
Carbohydrate Meal ◽  
Atrial Natriuretic

1. The renal function changes induced by dietary protein are thought to result from the activity of hormonal factors that remain as yet undefined. Since a meat meal and high dose atrial natriuretic factor (ANF) infusions have similar effects on glomerular filtration rate, natriuresis and kaliuresis, we decided to investigate the possibility that a protein meal could stimulate ANF activity. 2. We studied 10 normal volunteers who had a fixed protein and sodium intake for 7 days before the experiments. The subjects received a meat meal (1–1.5 g of protein/kg) and, on a separate occasion, a carbohydrate meal that had a similar caloric, sodium and potassium content. Diuresis was stimulated with water ingestion, and urine collections were obtained before the meals (baseline) and after the meals for a period of 3 h. Blood samples were obtained 30 min and 5 min before the meals and every hour for 3 h in the period after the meal. 3. The protein meal, but not the carbohydrate meal, was associated with parallel increments in plasma immunoreactive ANF (i-ANF), natriuresis, kaliuresis and glomerular filtration rate (estimated from creatinine clearances) which reached peak values 2–3 h after the meal. The mean increment of plasma i-ANF after the protein meal represented a twofold increase over baseline levels. 4. We conclude that ANF may participate in the physiological response to an oral protein load.

Native tubular fluid attenuates ANF-induced inhibition of tubuloglomerular feedback

1990 ◽  
Vol 258 (1) ◽  
pp. F189-F198 ◽  
Author(s):  
D. M. Pollock ◽  
W. J. Arendshorst
Keyword(s):  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Pressure Range ◽  
Tubuloglomerular Feedback ◽  
Fluid Delivery ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Flow Pressure ◽  
Stop Flow

The effect of atrial natriuretic factor [ANF-(1–28); 0.25 microgram.kg-1.min-1] on tubuloglomerular feedback (TGF) and the efficiency of renal blood flow (RBF) autoregulation was determined in anesthetized euvolemic rats. In microperfusion studies, ANF dramatically inhibited (greater than 80%) feedback-mediated decreases in single-nephron glomerular filtration rate (SNGFR) and stop-flow pressure (Psf) when Henle's loop was perfused at 0–48 nl/min with artificial fluid. The sigmoidal relationship between Psf and loop perfusion during control was shifted to a linear relation during ANF; reactivity was almost nonexistent and no inflection point could be discerned. ANF almost completely blocked maximum Psf and SNGFR responses to loop perfusion at rates greater than 24 nl/min. In contrast 30 nl/min loop perfusion with native proximal tubular fluid obtained during ANF infusion restored maximum TGF activity to 70% of control levels. During ANF administration, the paired Psf responses to native and artificial perfusate were significantly different (-5.3 vs. -0.8 mmHg, P less than 0.001), compared with similar responses during control conditions (-7.6 vs. -8.3 mmHg, P greater than 0.1). In free-flow studies, ANF increased proximally and distally measured SNGFR equally. The constancy of the proximal-distal SNGFR difference (10.3 vs. 9.3 nl/min) in the presence of increased distal fluid delivery suggests partial inhibition of TGF during ANF administration. ANF elevated Psf but did not affect basal RBF or the RBF autoregulatory index over an arterial pressure range of 130–70 mmHg. These results indicate that 1) RBF autoregulation is efficiently maintained during ANF infusion when preglomerular vessels are vasodilated and TGF is inhibited by approximately 30%; 2) an endogenous factor(s) in native proximal tubular fluid may attenuate ANF-induced inhibition of TGF; and 3) microperfusion studies using artificial fluid significantly overestimate the net in vivo effect of ANF on TGF.

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