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

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.

1984 ◽  
Vol 247 (5) ◽  
pp. F863-F866 ◽  
Author(s):  
J. C. Burnett ◽  
J. P. Granger ◽  
T. J. Opgenorth

Studies were performed in anesthetized dogs (n = 5) to determine the effects of synthetic atrial natriuretic factor on renal function and renin release. Intrarenal infusion of synthetic atrial natriuretic factor (ANF) (0.3 microgram X kg-1 X min-1) resulted in a transient increase in renal blood flow (126 +/- 8 to 148 +/- 11 ml/min). The duration of this transient vasodilation was 3.1 +/- 0.4 min. Continued infusion was followed by a slight decrease in renal blood flow (126 +/- 8 to 117 +/- 8 ml/min) and an increase in glomerular filtration rate (23.1 +/- 3.5 to 30.7 +/- 1.9 ml/min), with filtration fraction thus being increased (0.19 +/- 0.04 to 0.27 +/- 0.03). These hemodynamic alterations were associated with increases in fractional sodium excretion (0.6 +/- 0.2 to 5.8 +/- 0.8%), fractional potassium excretion (30.8 +/- 9.4 to 56.3 +/- 7.4%), fractional lithium excretion (32.2 +/- 7.1 to 60.3 +/- 5.7%), and fractional phosphate excretion (8.7 +/- 3.5 to 41.6 +/- 11.7%). Intrarenal infusion of synthetic ANF markedly suppressed renin secretion rate (295.5 +/- 84.6 to 17.2 +/- 10.6 ng/min) despite a slight reduction in arterial pressure (123 +/- 9 to 118 +/- 9 mmHg). Our studies demonstrate that synthetic ANF results in a marked natriuretic response that is in part mediated by an increase in glomerular filtration rate. The increase in fractional lithium and phosphate excretion suggests that this factor may also have an action on proximal tubule reabsorption. Further, these studies demonstrate that synthetic ANF markedly inhibits renin secretion.


1988 ◽  
Vol 254 (3) ◽  
pp. R453-R456 ◽  
Author(s):  
C. J. Showalter ◽  
R. S. Zimmerman ◽  
T. R. Schwab ◽  
B. S. Edwards ◽  
T. J. Opgenorth ◽  
...  

The present study in anesthetized dogs (n = 8) was designed to test the hypothesis that intrarenal angiotensin II (ANG II) attenuates the increase in sodium excretion in response to atrial natriuretic factor (ANF). To test this hypothesis, renal hemodynamic and excretory responses to systemically administered ANF (0.3 micrograms.kg-1.min-1) were assessed in the presence of ANG II infusion into the left kidney (ANG II K) at a nonpressor dose (1.5 ng.kg-1.min-1) and with an infusion of saline into the right kidney, the latter which served as control (CK). During ANF infusion, absolute increases in urinary sodium excretion (delta + 160.8 +/- 44.7 vs. delta + 369.4 +/- 56.9 mu eq/min, P less than 0.005) and fractional sodium excretion (delta + 2.55 +/- 0.62 vs. delta + 4.26 +/- 0.82%, P less than 0.03) were markedly attenuated in the ANG II K compared with CK. Glomerular filtration rate increased only in the CK. Urine osmolality decreased in both the ANG II K and CK. These studies demonstrate an attenuated natriuresis to ANF in the presence of intrarenally infused ANG II, which is associated with a blunted increase in glomerular filtration rate. These studies support the hypothesis that the renal hemodynamic and excretory responses to ANF are modulated by intrarenal ANG II.


1989 ◽  
Vol 257 (6) ◽  
pp. F1146-F1157 ◽  
Author(s):  
R. Mejia ◽  
J. M. Sands ◽  
J. L. Stephenson ◽  
M. A. Knepper

Atrial natriuretic factor (ANF) is a peptide hormone that increases renal NaCl and water excretion. Several renal sites of ANF action have been identified, but general agreement has not been reached concerning the quantitative contribution of each action to the natriuresis and diuresis. Using a five-nephron central core model of NaCl, urea, KCl, and water transport in the rat kidney, we have quantitatively evaluated the hypothetical effects on whole kidney function of three experimentally observed ANF actions: 1) inhibition of active NaCl absorption in the collecting duct, 2) inhibition of osmotic water permeability in the collecting duct, and 3) increased NaCl and water delivery out of the proximal convoluted tubule simulating an increase in glomerular filtration rate. The simulations show that inhibition of collecting duct active NaCl absorption by greater than or equal to 50% can increase NaCl and water excretion to levels that match experimental values. In addition, the model predicted that the urinary sodium concentration will increase to greater than plasma levels as observed experimentally. Simulated decreases in collecting duct water permeability predicted an increase in water excretion with little change in NaCl excretion. Simulated 2.5–5% increases in glomerular filtration rate also increased simulated NaCl and water excretion rates to experimentally observed levels in response to ANF. However, this action was less effective than inhibition of collecting duct active NaCl absorption in increasing the urinary NaCl concentration. We conclude that a combination of several actions are likely to account for the overall renal effect of ANF.


1991 ◽  
Vol 1 (9) ◽  
pp. 1081-1086
Author(s):  
J M Sands ◽  
J F Neylan ◽  
R A Olson ◽  
D P O'Brien ◽  
J D Whelchel ◽  
...  

Atrial natriuretic factor (ANF) ameliorates renal damage in animal models of acute ischemic renal failure. Consequently, ANF could blunt acute tubular necrosis related to ischemia that occurs frequently in cadaveric renal transplants. Ten pairs of cadaveric kidneys were transplanted into 20 recipients. Paired recipients received either alpha-human ANF (hANF) or vehicle alone in a prospective, double-blind protocol. Upon revascularization of the allograft, either hANF or vehicle was administered intravenously as a 50-micrograms bolus, followed by a 4-h infusion (0.1 microgram/kg/min). Glomerular filtration rate ([125I]iothalamate clearance) was measured between 4 and 7 days posttransplant and again between 14 and 21 days posttransplant. Serum creatinine was measured daily when patients were in the hospital, then twice weekly as patients were examined in the outpatient clinic. Between the groups, there was no significant difference in age of the recipients or donors, cold ischemia time, or histocompatibility leukocyte antigen match. Infusion of hANF had no adverse effects. When subjects receiving hANF were compared with those treated with vehicle alone, there were no significant differences in serum creatinine or glomerular filtration rate. Three hANF and four vehicle recipients required dialysis postoperatively. At 1 month posttransplant, 19 of 20 patients had functioning allografts; an allograft from one hANF recipient never functioned. It was concluded that hANF, when given by the protocol of this study, had no beneficial effect on the outcome of cadaveric renal transplantation in humans.


1986 ◽  
Vol 250 (4) ◽  
pp. F710-F714 ◽  
Author(s):  
M. G. Cogan

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.


1990 ◽  
Vol 78 (5) ◽  
pp. 481-485 ◽  
Author(s):  
S. C. Tam ◽  
L. S. Tang ◽  
C. K. Lai ◽  
M. G. Nicholls ◽  
R. Swaminathan

1. The increase in glomerular filtration rate after a protein meal is believed to be mediated by hormonal factors. Since natriuresis is often observed after a protein meal, it was postulated that the increase in glomerular filtration rate after a protein meal might be mediated by atrial natriuretic peptide. 2. Subjects were given a low, medium or high protein meal. Fluid intake was controlled so as to avoid significant extracellular fluid volume expansion. It was found that the creatinine clearance, the urea excretion, the fractional sodium excretion and the potassium excretion were elevated in all subjects after protein meals (P <0.05). These effects were not observed in subjects given a carbohydrate control meal. 3. The plasma atrial natriuretic peptide concentrations remained unchanged in all subjects except those given a high protein meal (P <0.05). There was no significant relationship between plasma atrial natriuretic peptide concentrations and creatinine clearance before or after a protein meal. 4. The data suggest that a high protein meal induces a minor increase in plasma atrial natriuretic peptide concentration, whereas a low or medium protein meal does not. It is unlikely that the change in creatinine clearance after a protein meal can be explained by a change in plasma atrial natriuretic peptide levels.


1988 ◽  
Vol 74 (1) ◽  
pp. 11-15 ◽  
Author(s):  
Bernardo Rodríguez-Iturbe ◽  
Josē Herrera ◽  
Rafael García

1. We studied the relationship between changes in glomerular filtration rate (GFR) determined as inulin clearance (CIn), and changes in renal blood flow (RBF), determined as p-aminohippurate clearance (CPAH), after the ingestion of a large (1.35±sem 0.04 g/kg, n = 9), moderate (1.08±0.03 g/kg, n = 10) or mild (0.55±0.02 g/kg, n = 8) protein load given as a meat meal. Control subjects (n = 10) received a carbohydrate meal. 2. CIn and CPAH increased after a protein meal. Two hours after eating the test meal, GFR levels were (mean ± sem) 160.0±13.8 (P < 0.05), 141 ± 7.69 and 127.8 ±9.07 ml/min in the groups that received a large, moderate and mild protein load, respectively. Peak CIn values after the meal were 211.6 ±sem 14.92 (P < 0.001), 177.5±10.88(P < 0.01)and 129.0±8.72 ml/min after a large, moderate and mild protein load, respectively. 3. At peak GFR levels after the meal, filtration fraction (FF) (CIn × 100/CPAH) increased significantly (P < 0.02) with the large and with the moderate protein load, but not with the mild protein load. 4. There was a significant (P < 0.001) positive relationship between increments of FF and increments of CIn, but not CPAH, whether the values were expressed as post-meal/pre-meal ratios or as absolute changes. 5. We conclude that hyperfiltration induced by a large protein load is associated with increments in GFR which are proportionally larger than the increments in RBF and, therefore, cannot be explained by simple vasodilatation. Factors capable of increasing FF operate in the physiological response to a protein meal.


2005 ◽  
Vol 360 (1-2) ◽  
pp. 205-207 ◽  
Author(s):  
Lorenz Risch ◽  
Christoph Saely ◽  
Ursula Reist ◽  
Kurt Reist ◽  
Martin Hefti ◽  
...  

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