Potentiation of the Natriuretic Effect of Atrial Natriuretic Factor (ANF) by Vasopressin (VP)

1986 ◽  
Vol 8 (6) ◽  
pp. 1309 ◽  
Author(s):  
E. H. Blaine ◽  
L. K. Nicolodi
1991 ◽  
Vol 260 (1) ◽  
pp. R217-R224 ◽  
Author(s):  
N. E. Bruun ◽  
P. Skott ◽  
J. Giese

The renal and endocrine effects of incremental infusions of 3 and 6 ng.kg-1.min-1 of exogenous atrial natriuretic factor (ANF)-(99-126) or placebo were investigated in 10 normal subjects. A 90-min basal period was followed by two 2-h infusion periods with urine collection in the last 90 min of each period. Plasma ANF concentration increased by 50 and 150%, respectively, from a basal value of 6.2 +/- 3.1 pmol/l. Plasma guanosine 3',5'-cyclic monophosphate concentration increased in parallel with ANF. Blood pressure and heart rate were unchanged, whereas hematocrit was stepwise increased. 51Cr-EDTA clearance (GFR) did not change, but ANF caused an increase in Li clearance (a measure of end-proximal fluid delivery), Na clearance, and urine flow compared with time-matched control values. These excretory effects of ANF were mainly due to prevention of the 20- to 50% decreases occurring in the placebo series. Calculated values of fractional proximal and distal tubular Na reabsorption decreased significantly. ANF caused a decrease in plasma concentrations of active renin and aldosterone, whereas renin substrate, angiotensin I, and angiotensin II concentrations were unaltered. A subtle increase in plasma concentrations of norepinephrine and epinephrine was observed during the ANF infusions. These data suggest that the natriuretic effect of ANF is caused by an increased fluid delivery from the proximal tubule in addition to a fall in fractional distal Na reabsorption.


1986 ◽  
Vol 250 (3) ◽  
pp. F520-F524 ◽  
Author(s):  
R. E. Sosa ◽  
M. Volpe ◽  
D. N. Marion ◽  
S. A. Atlas ◽  
J. H. Laragh ◽  
...  

The degree by which atrial natriuretic factor (ANF)-induced renal hemodynamic changes account for its natriuretic effect was determined by early clamp experiments in six anesthetized dogs. After control periods, perfusion pressure of the left kidney (LK) was reduced to 80-90 mmHg, and synthetic ANF (auriculin A) was infused intravenously (0.3 micrograms X min-1 X kg body wt). After recovery, furosemide (F) was administered as a bolus injection (1 mg/kg body wt). In the right kidney (RK), which served as a time control, ANF increased (P less than 0.05) glomerular filtration rate (GFR) 16 +/- 4% and Na excretion (UNa V) 261 +/- 63%, whereas it decreased urine osmolality (Uosm) 36 +/- 7% without changing free water clearance. ANF also increased diuresis (V) and kaliuresis (UKV). F produced qualitatively the same results without changing GFR. In the clamped LK, ANF failed to increase GFR (22 +/- 4 vs. 26 +/- 4 ml/min), UNaV (30 +/- 9 vs. 33 +/- 11 mueq/min), V, and UKV or to decrease Uosm (841 +/- 97 vs. 840 +/- 114 mosmol/kg H2O). F had similar effects in LK as in RK. The data demonstrate that the natriuretic effect of ANF is abolished when its renal hemodynamic actions are impeded. In addition, the results demonstrate that ANF antagonizes renal vasoconstriction in the dog. The results are consistent with the view that the ANF-induced natriuresis is due in great part to an increase in the filtered load of Na into a washed-out inner medulla.


Hypertension ◽  
1988 ◽  
Vol 12 (4) ◽  
pp. 450-456 ◽  
Author(s):  
C A Gaillard ◽  
H A Koomans ◽  
T J Rabelink ◽  
B Braam ◽  
P Boer ◽  
...  

1989 ◽  
Vol 257 (5) ◽  
pp. R1057-R1067
Author(s):  
E. Maher ◽  
P. Cernacek ◽  
M. Levy

Atrial natriuretic factor (ANF) (175 ng.kg-1.min-1) was administered to 14 normal, alert dogs and again after constriction of the thoracic vena cava. The average natriuresis observed in the dogs when they were normal was blunted by 55% when they developed ascites and were avidly retaining sodium. Of the 14 caval dogs, 7 showed a natriuretic response no different from the control phase while 7 showed no natriuresis at all in response to the ANF. Ten dogs were restudied when they entered a phase of sodium balance despite the persistence of ascites. All 10 dogs now responded to ANF, and 5 dogs previously not responding now showed a mean change of urinary sodium excretion rate (delta UnaV) of 204 mu eq/min. The two groups could not be differentiated in terms of plasma volume, systemic or renal hemodynamics, or plasma levels of renin and aldosterone. We conclude that there is reversible attenuation of the ANF natriuretic effect in 50% of chronic caval dogs, which disappears when they lose avidity for sodium retention.


1987 ◽  
Vol 16 (1) ◽  
pp. 63-77 ◽  
Author(s):  
John W. Jacobs ◽  
George P. Vlasuk ◽  
Michael Rosenblatt

1986 ◽  
Vol 113 (1_Suppl) ◽  
pp. S165-S166 ◽  
Author(s):  
G. WAMBACH ◽  
S. GÖTZ ◽  
G. SUCKAU ◽  
G. BÖNNER ◽  
W. KAUFMANN

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