Atrial natriuretic factor in dogs with one-kidney, one-clip Goldblatt hypertension

1987 ◽  
Vol 253 (6) ◽  
pp. H1623-H1627 ◽  
Author(s):  
K. M. Verburg ◽  
R. H. Freeman ◽  
D. Villarreal ◽  
M. W. Brands
Keyword(s):  
Arterial Pressure ◽  
Renal Artery ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Right Atrial ◽  
Maximal Response ◽  
Base Line ◽  
Natriuretic Factor ◽  
Renal Artery Constriction ◽  
Atrial Natriuretic

The temporal changes in the plasma concentration of immunoreactive atrial natriuretic factor (ANF) were studied in dogs (n = 5) before and after renal artery constriction to produce one-kidney, one-clip renovascular hypertension. Three days after renal artery constriction, circulating ANF increased from 34 +/- 7 to 344 +/- 129 pg/ml (P less than 0.05) in association with a 38-mmHg elevation of mean arterial pressure and increases in plasma renin and aldosterone levels. Plasma renin and aldosterone remained elevated for 9 days after renal artery constriction. Arterial pressure stabilized at this elevated level of 35-40 mmHg above base line for the duration of the 4 wk after renal artery constriction. Right atrial filling pressure did not change significantly (P greater than 0.05) after constriction of the renal artery. This observation suggests that volume expansion with right atrial distention is not the only stimulus for release of ANF in these hypertensive dogs. Plasma ANF remained significantly elevated above base-line levels for 7 days postconstriction even though a twofold decrease from the maximal response of 344 +/- 129 pg/ml on day 3 to 168 +/- 48 pg/ml on day 7 was observed during this same time interval. Plasma ANF continued to decrease toward prehypertensive levels throughout the remainder of the established phase of the hypertension lasting an additional 21 days of observation. The mechanisms for this observed pattern of plasma ANF are unclear but may involve changes in left atrial distention and stretch as a stimulus for hormone secretion with progression of the hypertension.

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.

Fetal cardiovascular, endocrine, and fluid responses to atrial natriuretic factor infusion

1989 ◽  
Vol 257 (3) ◽  
pp. R580-R587 ◽  
Author(s):  
R. A. Brace ◽  
L. A. Bayer ◽  
C. Y. Cheung
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Fetal Sheep ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The purpose of this study was to determine the effects of atrial natriuretic factor (ANF) in the fetus and to explore the interactions among the fetal cardiovascular, endocrine, and fluid responses to ANF. In 12 chronically catheterized fetal sheep at 130 +/- 1 (SE) days gestation, ANF was infused intravenously for 30 min at 14-300 ng.min-1.kg-1. Fetal arterial plasma ANF concentration increased by 174 to 5,410 pg/ml from a preinfusion value of 163 +/- 13 pg/ml. The clearance of ANF from the circulation was 122 +/- 28 ml.min-1.kg-1 and the half-life was 0.46 +/- 0.07 min. When plasma ANF was greater than 2,000 pg/ml, fetal arterial pressure decreased, venous pressure increased transiently, and heart rate was unchanged. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) increased with high ANF concentrations, while norepinephrine concentrations were unaffected. Fetal blood volume decreased in all fetuses, and urine flow increased significantly but not in every fetus. Blood and urine osmolalities did not change. On terminating the infusion, venous pressure and urine flow decreased below control, while blood volume and arterial pressure remained reduced. Plasma AVP concentration increased further, and this was accompanied by an increase in urine osmolality. Thus the most consistent effect of ANF in the fetus was a reduction in blood volume, which was independent of urine flow changes. Other cardiovascular, endocrine, and fluid responses to ANF as well as interactions among them appeared to occur largely at supraphysiological concentrations and may be secondary to the changes in blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Aldosterone and renin inhibition by physiological levels of atrial natriuretic factor

1988 ◽  
Vol 254 (6) ◽  
pp. R1011-R1016 ◽  
Author(s):  
M. W. Brands ◽  
R. H. Freeman
Keyword(s):  
Plasma Renin Activity ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Base Line ◽  
Lower Plasma ◽  
Aldosterone Secretion ◽  
Low Sodium Diet ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

This study was designed to examine, in the rat, the inhibition of renin release and aldosterone secretion by physiological plasma levels of atrial natriuretic factor (ANF). Intravascular volume expansion over 30 min with donor blood equal to 3% body weight increased plasma ANF concentration from a base line of 216 +/- 28 to 1,590 +/- 240 pg/ml (P less than 0.001) in sodium-replete rats. Basal plasma ANF levels were decreased to 125 +/- 9 pg/ml in animals fed a low-sodium diet, and the infusion of synthetic ANF into separate groups of these rats at doses of 15 or 45 ng.kg-1.min-1 elevated plasma ANF to 346 +/- 38 and 720 +/- 96 pg/ml, respectively (P less than 0.001 for both values). Infusion of ANF at 15 ng.kg-1.min-1 resulted in a significantly lower plasma renin activity [30 +/- 3 vs. 69 +/- 5 ng angiotensin I (ANG I).ml-1.h-1, P less than 0.05], but there was no difference in aldosterone secretion between control and infused groups (7.00 +/- 0.49 vs. 7.29 +/- 0.95 ng/min, P greater than 0.05). However, the higher ANF dose of 45 ng.kg-1.min-1 did reduce aldosterone secretion approximately 40% to 4.18 +/- 0.36 ng/min (P less than 0.001) with no further suppression in plasma renin activity. In sodium-replete rats, infusion of ANF at 45 ng.kg-1.min-1 resulted in lower plasma renin activity compared with the control noninfused group (14 +/- 4 vs. 22 +/- 2 ng ANG I.ml-1.h-1, P less than 0.05), but aldosterone secretion was not different (P greater than 0.05) between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

DOCA administration and atrial natriuretic factor in dogs with chronic heart failure

1989 ◽  
Vol 257 (3) ◽  
pp. H739-H745 ◽  
Author(s):  
D. Villarreal ◽  
R. H. Freeman ◽  
M. W. Brands
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Base Line ◽  
Cardiac Reserve ◽  
Natriuretic Factor ◽  
High Output Heart Failure ◽  
High Output ◽  
Atrial Natriuretic

The chronic reserve for the secretion of atrial natriuretic factor (ANF) was studied in conscious dogs with an arteriovenous (a-v) fistula, a model of high-output heart failure. After the first 7 days of marked sodium retention after creation of the a-v fistula, the animals regained sodium balance for the subsequent 3 wk. This compensatory natriuresis occurred in the presence of significant increases in right atrial pressure and was associated with marked and sustained elevations in plasma ANF and with the return of plasma renin and aldosterone to base-line values. The cardiac reserve for ANF secretion was further evaluated in these dogs with compensated high-output heart failure during additional progressive elevations in cardiac filling pressures induced by 3 wk of deoxycorticosterone acetate (DOCA) administration. During the DOCA regimen, plasma ANF increased an additional twofold from its high base line. Arterial blood pressure increased by 6–12 mmHg, and plasma renin activity was suppressed. However, the animals consistently retained sodium, and the high plasma levels of ANF were unable to counterbalance the sodium-retaining actions of DOCA. After termination of DOCA, the dogs exhibited a marked natriuresis, and all the hemodynamic and hormonal parameters returned to pre-DOCA control levels. This longitudinal study demonstrates that the cardiac reserve for chronic ANF secretion is well maintained in dogs with an a-v fistula during progressive cardiac volume overload. The present results suggest that the ANF endocrine system may represent one chronic compensatory mechanism to achieve sodium balance in heart failure when there is concomitant normalization of the renin-aldosterone system.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic factor attenuates carotid baroreflex-mediated cardioacceleration in humans

1988 ◽  
Vol 254 (4) ◽  
pp. R590-R594 ◽  
Author(s):  
T. J. Ebert ◽  
A. W. Cowley
Keyword(s):  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Base Line ◽  
Sinus Arrhythmia ◽  
Carotid Baroreceptor ◽  
Natriuretic Factor ◽  
Carotid Baroreflex ◽  
Neck Pressure ◽  
Atrial Natriuretic

We tested the hypothesis that infusions of atrial natriuretic factor (ANF) attenuate carotid baroreflex-mediated tachycardia in humans. The afferent profile from carotid baroreceptors was altered by repeated, intermittent random applications of neck suction (40 mmHg) and neck pressure (20 mmHg) to healthy volunteers during supine control and during infusions of 15 (n = 6) or 25 ng.kg-1.min-1 (n = 9) of alpha-human ANF or during placebo (n = 9). ANF infusions resulted in five- and eightfold increases of plasma ANF, which did not alter base-line cardiac interval, blood pressure, respiratory sinus arrhythmia, plasma renin activity, vasopressin, or norepinephrine but did reduce central venous pressure. Reflex bradycardic responses were unaltered during these infusions. Reflex tachycardic responses to carotid compression were significantly blunted (up to 40%) during infusions of ANF and were unchanged during placebo. These responses may be due to a sensitization of cardiac receptors and augmentation of cardiac-vagal afferent traffic by ANF, which diminishes reflex cardiac-sympathetic outflow during carotid baroreceptor unloading.

Aldosterone and renin inhibition by atrial natriuretic factor in potassium-loaded rats

1989 ◽  
Vol 257 (6) ◽  
pp. R1423-R1428
Author(s):  
M. W. Brands ◽  
R. H. Freeman
Keyword(s):  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
Normal Diet ◽  
Base Line ◽  
Aldosterone Secretion ◽  
Natriuretic Factor ◽  
Renin Inhibition ◽  
Potassium Loading ◽  
Atrial Natriuretic

This study was designed to determine the effects of synthetic rat atrial natriuretic factor (ANF) on plasma renin activity (PRA) and aldosterone secretion in separate groups of normal and potassium-loaded anesthetized rats. Control rats were fed a normal diet of sodium and potassium and had base-line levels of PRA and aldosterone secretion of 25 +/- 3 ng angiotensin I (ANG I).ml-1.h-1 and 0.56 +/- 0.09 ng/min, respectively. Chronic oral potassium loading for 10 days elevated the plasma potassium concentration, stimulated aldosterone secretion to 1.80 +/- 0.18 ng/min (P less than 0.05), and attenuated PRA to 13 +/- 2 ng ANG I.ml-1.h-1 (P less than 0.05). Infusion of ANF at 45 ng.kg-1.min-1 in potassium-loaded rats lowered aldosterone secretion to 1.32 +/- 0.21 ng/min (P less than 0.05) but did not significantly reduce PRA (11 +/- 2 ng ANG I.ml-1.h-1 (P greater than 0.05). A higher ANF infusion dose of 100 ng.kg-1.min-1 produced a further decrement in aldosterone secretion to 1.15 +/- 0.26 ng/min (P less than 0.05) and also reduced PRA to 3 +/- 1 ng ANG I.ml-1.h-1 (P less than 0.05). In the control rats, aldosterone secretion and PRA were decreased significantly during infusion with both low and high ANF doses. Base-line arterial pressures among experimental groups were not different (P greater than 0.05) and did not change during infusion of ANF in any group. These results indicate that ANF can inhibit chronic potassium-stimulated aldosterone secretion in the rat independently of its inhibitory actions on renin release.

Effects of hypoxia and hypercapnia on atrial natriuretic factor and plasma renin activity in conscious dogs

1989 ◽  
Vol 76 (3) ◽  
pp. 249-254 ◽  
Author(s):  
Jean-Paul Clozel ◽  
Claude Saunier ◽  
Denise Hartemann ◽  
Mustapha Allam ◽  
Walter Fischli
Keyword(s):  
Atrial Natriuretic Factor ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Random Order ◽  
Respiratory Alkalosis ◽  
Right Atrial ◽  
Natriuretic Factor ◽  
Left And Right ◽  
Chronically Instrumented Dogs ◽  
Atrial Natriuretic

1. The aim of the present study was to assess the effects of hypercapnia or hypoxia on plasma concentrations of atrial natriuretic factor (ANF) in conscious unrestrained dogs. 2. For this purpose, chronically instrumented dogs were exposed in a random order to either room air, or to an atmosphere containing 21% O2/10% CO2/69% N2 to produce hypercapnia, or 10% O2/3% CO2/87% N2 to produce hypoxia without respiratory alkalosis. 3. Plasma concentrations of ANF did not change significantly during hypoxia. 4. In contrast, during hypercapnia, plasma concentrations of ANF increased by more than 100% and returned to baseline at the end of hypercapnia. 5. Hypercapnia, but not hypoxia, induced an increase in left atrial and central venous pressures. 6. We conclude that hypercapnia increases plasma ANF concentration, and that this increase may be secondary to an increase of the left and right atrial pressures. These phenomena may explain the increase in diuresis and natriuresis which has been described during hypercapnia.

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.

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