Role of the renal nerves in the response by atrial natriuretic factor to acute volume expansion

1991 ◽  
Vol 9 (6) ◽  
pp. S252
Author(s):  
Paulien Wijnmaalen ◽  
Carla Sala ◽  
Simonetta Genovesi ◽  
Giorgio Ardeleani ◽  
Giuseppe Protasoni ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Renal Nerves ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Role of the renal nerves in the response by atrial natriuretic factor to acute volume expansion

1991 ◽  
Vol 9 ◽  
pp. S252
Author(s):  
Paulien Wijnmaalen ◽  
Carla Sala ◽  
Simonetta Genovesi ◽  
Giorgio Ardeleani ◽  
Giuseppe Protasoni ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Renal Nerves ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The contribution of atrial natriuretic factor to acute volume natriuresis in rats

1987 ◽  
Vol 253 (6) ◽  
pp. F1129-F1135 ◽  
Author(s):  
R. W. Barbee ◽  
N. C. Trippodo
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Urinary Sodium Excretion ◽  
Right Atrial ◽  
Natriuretic Factor ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic

To explore the role of atrial natriuretic factor (ANF) in acute volume-expansion natriuresis, right atrial pressure (RAP), mean arterial pressure (MAP), rate of urinary sodium excretion (UNaV), and plasma immunoreactive ANF (IR-ANF) were measured in anesthetized, open-chest rats. All groups received 33% blood volume expansion with whole blood in 15 min. RAP was not allowed to increase in one group by using a caval snare. MAP was controlled in a second group with the use of an aortic snare. A third group (RAP-controlled ANF) with control of RAP received rat ANF (99-126) at doses designed to mimic the IR-ANF measured in the MAP-controlled rats. IR-ANF was similar 5 min after blood infusion in rats exhibiting increased RAP (490 +/- 111 pg/ml) and in those without increased RAP but receiving ANF infusion (447 +/- 44 pg/ml); this was also true at 45 min after blood infusion (232 +/- 44 vs. 263 +/- 27 pg/ml). IR-ANF in rats with constant RAP (without ANF infusion) remained low throughout the experiment (61 +/- 10 and 74 +/- 10 pg/ml). UNaV increased only in the MAP-controlled and ANF-infused groups, but peak responses occurred 15-30 min after the onset of volume expansion in the former, and 60-75 min in the latter. Thus, factors other than ANF mostly accounted for the immediate natriuresis after volume expansion, whereas ANF predominated after a delayed period. The results suggest that increased plasma ANF accounted for at least 34% of the observed natriuretic response to acute volume expansion in anesthetized rats.

Role of atrial natriuretic factor in the natriuresis of acute volume expansion

1987 ◽  
Vol 252 (5) ◽  
pp. R921-R924 ◽  
Author(s):  
A. A. Khraibi ◽  
J. P. Granger ◽  
J. C. Burnett ◽  
K. R. Walker ◽  
F. G. Knox
Keyword(s):  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
Sprague Dawley ◽  
Volume Loading ◽  
Fourfold Increase ◽  
Natriuretic Factor ◽  
Fractional Excretion Of Sodium ◽  
Atrial Natriuretic

The quantitative role of atrial natriuretic factor (ANF) in mediating the natriuresis induced by acute volume loading was determined in these studies. Plasma level of ANF (PANF), glomerular filtration rate (GFR), and renal excretory responses were measured in three groups of anesthetized Sprague-Dawley rats. In one group of rats (n = 8), acute volume expansion was established by intravenous infusion of saline (5% body wt) over a period of 30 min. A second group of rats (n = 13) was infused with synthetic ANF (2 micrograms X kg-1 X h-1 iv) to mimic the high PANF observed during acute volume loading. A third group (n = 13) served as control. PANF was similar and significantly elevated (P less than 0.05) in volume-expanded and ANF-infused groups compared with control. In control rats, PANF measured 122.0 +/- 12.1 pg/ml, whereas it averaged 389.4 +/- 30.3 pg/ml for volume-expanded and 368.1 +/- 22.3 pg/ml for ANF-infused rats. GFR was also comparable and significantly increased (P less than 0.05) in volume-expanded and ANF-infused groups compared with control rats. Infusion of ANF at a dose to mimic PANF obtained during acute volume expansion resulted in a fourfold increase in the fractional excretion of sodium. The results of these studies suggest that ANF may play an important quantitative role in promoting natriuresis during acute volume expansion.

Role of Atrial Natriuretic Factor, Hemodynamic Changes and Renal Nerves in the Renal Effects of Intraperitoneal Morphine in Conscious Rats

1997 ◽  
Vol 20 (1) ◽  
pp. 18-24 ◽  
Author(s):  
Olga Flores ◽  
Luis A. Camera ◽  
Alfonso Hergueta ◽  
Belén Gallego ◽  
Fernando Pérez Barriocanal ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Renal Nerves ◽  
Hemodynamic Changes ◽  
Renal Effects ◽  
Conscious Rats ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Role of potassium channels in stretch-promoted atrial natriuretic factor secretion

2009 ◽  
Vol 3 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Tsuneo Ogawa ◽  
Monica Forero ◽  
Patrick G. Burgon ◽  
Mercedes L. Kuroski de Bold ◽  
Tina Georgalis ◽  
...  
Keyword(s):  
Potassium Channels ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Factor Secretion ◽  
Atrial Natriuretic

Neural influences on renal responses to acute volume expansion in rats with heart failure

1996 ◽  
Vol 271 (4) ◽  
pp. H1441-H1448 ◽  
Author(s):  
K. P. Patel ◽  
P. L. Zhang ◽  
P. K. Carmines
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Renal Nerve ◽  
Natriuretic Factor ◽  
Renal Nerve Activity ◽  
Neural Influences ◽  
Renal Responses ◽  
Renal Sympathetic ◽  
Atrial Natriuretic

Experiments were performed to test the postulate that neural influences underlie the suppressed excretory response to acute volume expansion (VE) typically observed 3-4 wk after myocardial infarction to induce chronic heart failure (CHF). Responses to VE were assessed in innervated (intact) and denervated (DNX) kidneys of anesthetized CHF rats and sham-operated controls. CHF rats exhibited blunted natriuretic responses to VE in both intact kidneys (35% of sham response) and DNX kidneys (55% of sham DNX response). CHF rats also displayed suppressed excretory responses to atrial natriuretic factor (0.25 microgram.kg-1.min-1 iv) in both intact kidneys (74% of sham response) and DNX kidneys (63% of sham DNX response). Additional experiments confirmed that the compliance of the venoatrial junction did not differ between sham rats (52 +/- 2 mmHg/microliter) and CHF rats (54-2 mmHg/microliter). The observations support the contention that both tonic renal sympathetic renal nerve activity and suppressed renal atrial natriuretic factor responsiveness likely contribute to the blunted excretory response to VE during CHF.

Central effects of atrial natriuretic factor on renal salt excretion

1991 ◽  
Vol 261 (2) ◽  
pp. F354-F359 ◽  
Author(s):  
P. Rohmeiss ◽  
G. Demmert ◽  
T. Unger
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Nerves ◽  
Urinary Flow ◽  
Renal Nerve ◽  
Ureteral Catheter ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Atrial natriuretic factor (ANF) has been localized in periventricular brain areas involved in cardiovascular and fluid control. We investigated the effect of intracerebroventricular (icv) ANF (alpha-rat atriopeptin III) on renal sodium excretion in unilaterally nephrectomized, conscious unrestrained rats fitted with a chronic ureteral catheter. Isotonic NaCl (1 ml/h) was infused intravenously. ANF injected at doses (icv) of 1 ng (n = 6), 100 ng (n = 7), and 1 microgram (n = 7) reduced urinary sodium excretion (all values mumol/45 min, means +/- SE) from 111.6 +/- 24.4 to 83 +/- 20 (P less than 0.05), from 96.9 +/- 25.2 to 55 +/- 14 (P less than 0.01), and from 90.8 +/- 14.2 to 51 +/- 9 (P less than 0.01), respectively, whereas urinary flow rate did not change. The antinatriuretic effect was immediate in onset and lasted for greater than or equal to 60 min. Blood pressure remained unaltered. ANF (100 ng icv) increased efferent sympathetic renal nerve activity (+36%; n = 6, P less than 0.05), plasma renin activity (4.6 +/- 0.6 to 7.5 +/- 0.5 pmol angiotensin I.ml-1.h-1; n = 9, P less than 0.01), plasma angiotensin II (68.7 +/- 2.5 to 84.7 +/- 3.4 fmol/ml; n = 8, P less than 0.01), and aldosterone (22.3 +/- 3.6 to 37.2 +/- 4.0 ng/ml; n = 9, P less than 0.02). Renal denervation reduced the antinatriuretic effect of ANF by 37%. We conclude that brain ANF has antinatriuretic actions, which may be partly explained by activation of renal nerves.

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