Effects of angiotensin II on plasma atrial natriuretic factor in nonpregnant and pregnant ewes

1995 ◽  
Vol 73 (5) ◽  
pp. 644-650 ◽  
Author(s):  
L. Fan ◽  
D. Javeshghani ◽  
S. Mukaddam-Daher ◽  
Z. Guan ◽  
B. S. Nuwayhid ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Pregnant Sheep ◽  
Nitroprusside Infusion ◽  
Atrial Natriuretic

The release of atrial natriuretic factor (ANF) is primarily determined by atrial stretch, but may also be modulated by circulating angiotensin II (AngII). During pregnancy, the circulating concentrations of both ANF and AngII are increased. To further define possible effects of AngII on ANF release, four doses of AngII (0.5, 5, 20, 40 ng∙kg−1∙min−1) were intravenously infused into five nonpregnant and five pregnant (105–140 days of gestation) ewes alone and during the simultaneous infusion of sodium nitroprusside at doses sufficient to abolish the pressor effects of AngII. Mean arterial pressure (MAP) was increased from 80 ± 2 to a maximum of 121 ± 5 mmHg (1 mmHg = 133.3 Pa) in nonpregnant ewes (p < 0.01) and from 79 ± 2 to 116 ± 4 mmHg in pregnant ewes (p < 0.01) over the range of AngII infusion. MAP was unaltered during AngII plus nitroprusside infusion, averaging 78 ± 3 mmHg in nonpregnant ewes and 80 ± 2 mmHg in pregnant ewes. Basal ANF was higher (p < 0.01) in pregnant sheep than in nonpregnant sheep. With AngII infusion alone, plasma ANF was increased from 13 ± 2 to 42 ± 4 fmol/mL in nonpregnant ewes (p < 0.01) and from 23 ± 5 to 72 ± 16 fmol/mL in pregnant ewes (p < 0.01). However, during AngII plus nitroprusside infusion, the increases in plasma ANF observed were completely abolished in both nonpregnant and pregnant ewes. These results suggest that AngII does not have a direct stimulatory effect on ANF release but rather that the increase in plasma ANF is a consequence of the pressor effects of AngII. This response does not appear to be altered during ovine pregnancy.Key words: angiotensin II, atrial natriuretic factor, nitroprusside, mean arterial pressure.

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.

Control of atrial natriuretic factor by right and left atrial distension in pregnant sheep

1995 ◽  
Vol 268 (6) ◽  
pp. R1411-R1417
Author(s):  
D. Javeshghani ◽  
S. Mukaddam-Daher ◽  
L. Fan ◽  
Z. Guan ◽  
J. Gutkowska ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Natriuretic Factor ◽  
Pregnant Sheep ◽  
Vascular Catheters ◽  
The Right ◽  
Left Atrial Distension ◽  
Atrial Natriuretic

Previous studies of the atrial stretch-atrial natriuretic factor (ANF) relationship during pregnancy have employed volume expansion and measured only right atrial pressure (RAP). Consequently, we studied nonpregnant (n = 7) and 115- to 125-day pregnant (n = 7) sheep and assessed the ANF response to changes of RAP and left atrial pressure (LAP) induced by graded balloon inflation. Ewes prepared with vascular catheters and atrial balloons were studied after recovery from preparatory surgical procedures. The basal levels of mean arterial pressure (MAP, 83 +/- 3 mmHg), RAP (2.1 +/- 0.7 mmHg), LAP (4.7 +/- 0.9 mmHg), and heart rate (HR, 102 +/- 6 beats/min) were similar in nonpregnant and pregnant sheep. Pregnancy also resulted in elevation of ANF concentration from 25 +/- 6 to 57 +/- 4 fmol/ml. With right atrial distension, the RAP-ANF relationships were similar in both nonpregnant and pregnant sheep, with a 10-mmHg increase in RAP increasing ANF by an average of 95 +/- 9 fmol/ml. In nonpregnant sheep, the LAP-ANF relationship was more responsive than RAP-ANF because a 10-mmHg increase in LAP resulted in a 193 +/- 10 fmol/ml increase in ANF. Moreover, during pregnancy, the LAP-ANF relationship was significantly more sensitive because a 10-mmHg increase in LAP resulted in a 433 +/- 15 fmol/ml elevation of ANF. These data demonstrate that plasma ANF levels are more responsive to distension of the left atria than to the right. More importantly, the ANF response to left, but not right, atrial distension is enhanced by pregnancy.

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.

Effects of sodium pump inhibition on the relaxation induced by synthetic Atrial Natriuretic Factor (ANF) and sodium nitroprusside

1985 ◽  
Vol 10 ◽  
pp. 110-112
Author(s):  
Michel Auguet ◽  
Sylvie Delaflotte ◽  
Ricardo Garay ◽  
Marc Cantin ◽  
François Clostre ◽  
...  
Keyword(s):  
Sodium Nitroprusside ◽  
Atrial Natriuretic Factor ◽  
Sodium Pump ◽  
Natriuretic Factor ◽  
Sodium Pump Inhibition ◽  
Atrial Natriuretic

Interaction of atrial natriuretic factor and angiotensin II in proximal HCO3- reabsorption

1992 ◽  
Vol 262 (2) ◽  
pp. F303-F308 ◽  
Author(s):  
G. N. Gomes ◽  
M. M. Aires
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Control Group ◽  
Ang Ii ◽  
Half Time ◽  
Capillary Perfusion ◽  
Perfusion Fluid ◽  
Natriuretic Factor ◽  
Peritubular Capillaries ◽  
Atrial Natriuretic

Bicarbonate reabsorption was evaluated by the acidification kinetics technique in middle proximal tubule in Munich-Wistar rats. Atrial natriuretic factor (ANF) and angiotensin II (ANG II) were infused into the jugular vein (ANF, 0.5 microgram.min-1.kg-1 after a prime of 10 micrograms/kg; ANG II, 20 ng.min-1.kg-1) or added to luminal or peritubular perfusion fluid (10(-6) M ANF; 10(-12) M ANG II). In the presence of ANF, in each condition, no significant differences in net HCO3- reabsorption or in acidification half time were observed compared with the control group. In the presence of ANG II, a significant increase in HCO3- reabsorption was observed, expressed by a fall in acidification half time from a mean of 4.75 +/- 0.20 (n = 86) to 2.47 +/- 0.18 s (n = 32) in systemically infused rats or to 2.30 +/- 0.15 s (n = 35) in luminally perfused tubules and from 4.57 +/- 0.32 (n = 44) to 2.04 +/- 0.10 s (n = 50) during capillary perfusion. However, when ANG II was systemically infused or perfused in lumen or in peritubular capillaries, addition of ANF to lumen or capillaries by perfusion or systemic infusion abolished the effects observed with ANG II alone. These studies confirm that ANG II stimulates proximal HCO3- reabsorption and show that ANF alone does not affect this process, but impairs the stimulation caused by ANG II.

Effect of atrial natriuretic factor on renal hemodynamics in the rat

1986 ◽  
Vol 251 (5) ◽  
pp. F795-F801 ◽  
Author(s):  
D. M. Pollock ◽  
W. J. Arendshorst
Keyword(s):  
Arterial Pressure ◽  
Atrial Natriuretic Factor ◽  
Renal Hemodynamics ◽  
Maximal Response ◽  
Water Excretion ◽  
Excretory Function ◽  
Routes Of Administration ◽  
Natriuretic Factor ◽  
Renal Vascular ◽  
Atrial Natriuretic

Clearance experiments were conducted to determine the effects of atrial natriuretic factor (ANF) on renal hemodynamics and excretory function in anesthetized, euvolemic Munich-Wistar rats. Intra-aortic infusions of synthetic ANF (28 amino acids) at 7.5 and 15 micrograms X kg-1 X h-1 produced dose-related increases in absolute and fractional sodium and water excretion under steady-state conditions; renal blood flow (RBF) was unchanged, whereas mean arterial pressure significantly decreased but remained within the autoregulatory range. An apparent maximal response was elicited by 15 micrograms X kg-1 X h-1 as 30 micrograms X kg-1 X h-1 produced a similar increase in urine flow and sodium excretion. ANF infusion at 30 micrograms X kg-1 X h-1 produced no transient or sustained changes in RBF (electromagnetic flow probe). Renal vascular resistance was significantly decreased in parallel with reductions in arterial pressure; ANF-induced changes in resistance can be explained by autoregulatory adjustments. In another series, intra-aortic vs. intravenous infusion of ANF (7.5 micrograms X kg-1 X h-1) were compared in the same animal; the diuretic and natriuretic response to ANF was similar with the two routes of administration. We observed no consistent changes in glomerular filtration rate (GFR). Our results indicate that the diuretic and natriuretic effects of synthetic ANF in the rat do not require an increase in RBF or GFR.

Sign in / Sign up

Export Citation Format

Share Document