Role of prostaglandins in mediating the renal effects of atrial natriuretic factor.

The potential role of atrial natriuretic factor (ANF) in the renal response to head-out water immersion (WI) was studied. Five female mongrel dogs, trained to stand for 100 min in air followed by 100 min of thermoneutral WI at 37 degrees C or 200 min in air (timed control, TC), were chronically instrumented with arterial and venous catheters. The animals were hydrated with a volume of 0.45% NaCl solution equivalent to 2% of their body weight. Prehydration levels of arterial ANF were 243 +/- 15 (SE), and venous ANF levels were 211 +/- 21 pg/ml. WI resulted in an increase in urine flow from 0.7 +/- 0.1 ml/min to a peak flow of 2.2 +/- 0.3 ml/min (P less than 0.05). On immersion, plasma venous and arterial ANF levels increased significantly by 29 and 21% from the preimmersion values of 183 +/- 14 and 222 +/- 20 pg/ml, respectively. The arterial-venous difference for plasma ANF was maintained at 35 +/- 14 pg/ml (P less than 0.05) during WI; therefore venous sampling may suffice as a measure of circulating ANF levels. Sodium excretion increased linearly during WI to a peak value of 228 +/- 32 mu eq/min from a base line of 52 +/- 12 mu eq/min (P less than 0.05). These data indicate that peripheral tissues extract ANF and that WI is a physiological stimulus for the release of ANF. However, the time course and magnitude of the changes in plasma ANF and urine sodium excretion during WI are not comparable, and other mechanisms are likely responsible for the WI natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

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Responses of vasoactive hormones in congestive cardiac failure

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-268 ◽

1987 ◽

Vol 65 (8) ◽

pp. 1706-1711 ◽

Cited By ~ 9

Author(s):

C. I. Johnston ◽

L. F. Arnolda ◽

K. Tsunoda ◽

P. A. Phillips ◽

G. P. Hodsman

Keyword(s):

Heart Failure ◽

Cardiac Failure ◽

Atrial Natriuretic Factor ◽

Peripheral Resistance ◽

Congestive Cardiac Failure ◽

Renin Angiotensin ◽

Natriuretic Factor ◽

Vasoactive Hormones ◽

Atrial Natriuretic

Congestive cardiac failure causes activation of various neurohumoral responses that increase total peripheral resistance and promote salt and water retention. These effects increase blood pressure and organ perfusion in the short term, but ultimately cause further cardiac decompensation by increasing ventricular afterload and cardiac work. The role of the renin–angiotensin–aldosterone system and the catecholamines is partially understood, and blockade of these systems as a treatment of heart failure is now established. The role of vasopressin in heart failure is more controversial, but there is now compelling evidence that vasopressin may have important vasoconstrictor actions in addition to its fluid retaining properties. Atrial natriuretic factor is a newly described cardiac hormone released from the atrium. Atrial natriuretic factor causes natriuresis, diuresis, vasodilatation, suppression of thirst, and suppression of both renin and aldosterone. These actions largely counteract the effects of the renin–angiotensin system and vasopressin. Plasma atrial natriuretic factor has been reported to be markedly elevated in human and experimental heart failure, and may act to limit the neurohumoral response to reduced cardiac output. This review summarizes our understanding of the vasoactive hormones and reports experimental evidence supporting a pathophysiological role for vasopressin and atrial natriuretic factor in congestive cardiac failure.

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Renal effects of atrial natriuretic factor during control of the renin-angiotensin system in anesthetized dogs.

Circulation Research ◽

10.1161/01.res.62.3.506 ◽

1988 ◽

Vol 62 (3) ◽

pp. 506-514 ◽

Cited By ~ 7

Author(s):

A A Seymour ◽

E K Mazack

Keyword(s):

Atrial Natriuretic Factor ◽

Renin Angiotensin System ◽

Angiotensin System ◽

Renal Effects ◽

Renin Angiotensin ◽

Natriuretic Factor ◽

Anesthetized Dogs ◽

Atrial Natriuretic

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Attenuation of renal effects of atrial natriuretic factor during rat pregnancy

AJP Renal Physiology ◽

10.1152/ajprenal.1995.268.3.f416 ◽

1995 ◽

Vol 268 (3) ◽

pp. F416-F422 ◽

Cited By ~ 4

Author(s):

S. Omer ◽

S. Mulay ◽

P. Cernacek ◽

D. R. Varma

Keyword(s):

Atrial Natriuretic Factor ◽

Collecting Duct ◽

Sprague Dawley ◽

Pregnant Rats ◽

Renal Effects ◽

Natriuretic Factor ◽

Sprague Dawley Rats ◽

Collecting Duct Cells ◽

Renal Responses ◽

Atrial Natriuretic

The influence of pregnancy on renal responses to atrial natriuretic factor (ANF) was determined in urethane-anesthetized Sprague-Dawley rats. Infusions of ANF caused a significantly greater increase in urinary excretion of fluid, sodium, and potassium in virgin than in pregnant (13-15 days and 21 days) rats. Guanosine 3',5'-cyclic monophosphate (cGMP) excretion, mean arterial pressure, plasma immunoreactive ANF, and glomerular filtration rate (GFR) following ANF infusions were not different in virgin and gravid rats, although increments in GFR over basal were greater in virgin than in gravid animals. Renal responses to ANF normalized during postpartum and were attenuated by progesterone treatment of virgin rats. Natriuretic effects of infusions of ANF plus ANF-(4-23) (a ligand for clearance receptors) or of ANF plus thiorphan (an endopeptidase inhibitor) in virgin and pregnant rats did not differ; ANF-(4--23) and thiorphan alone caused greater natriuresis in pregnant than in virgin rats. Effects of ANF on cGMP production by collecting duct cells isolated from virgin and pregnant rats did not differ. We concluded that the attenuation in the renal effects of ANF during pregnancy might be mediated by progesterone by an increase in the intrarenal metabolism of ANF and might reflect physiological adjustment to facilitate fluid/electrolyte expansion.

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Low-dose endothelin-1 potentiates volume-induced secretion of atrial natriuretic factor

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.263.3.h939 ◽

1992 ◽

Vol 263 (3) ◽

pp. H939-H944 ◽

Cited By ~ 3

Author(s):

J. Donckier ◽

C. Hanet ◽

L. Galanti ◽

L. Stoleru ◽

H. Van Mechelen ◽

...

Keyword(s):

Heart Rate ◽

Atrial Natriuretic Factor ◽

Left Atrial ◽

Low Dose ◽

Endothelin 1 ◽

Natriuretic Factor ◽

Free Intracellular Calcium ◽

Phosphoinositide Pathway ◽

Atrial Natriuretic

To evaluate the role of calcium in volume-induced secretion of atrial natriuretic factor (ANF), effects of verapamil and endothelin-1 (ET-1), both known to influence free intracellular calcium, were studied during saline infusion in seven conscious instrumented dogs. Fifteen minutes after intravenous injection of placebo or verapamil (0.25 mg/kg) or during continuous ET-1 infusion (at 5 ng.kg-1.min-1), saline (10% body wt) was infused during 40 min. Saline produced a rise (P less than 0.001) of plasma ANF from 28.1 +/- 6.3 to 50.4 +/- 12.9 pM after placebo, from 30.2 +/- 6.1 to 51.1 +/- 8.5 pM after verapamil, and from 31.2 +/- 6.1 to 81.0 +/- 12.9 pM with ET-1. This increase was comparable after placebo and verapamil, but was 80% greater with ET-1 (P less than 0.02). Plasma ET-1, unchanged after placebo, rose (P less than 0.001) from 1.7 +/- 0.5 to 38.3 +/- 9.2 pM with ET-1. In the three experiments, heart rate and left atrial pressure (LAP) increased (P less than 0.001) similarly. The linear relation between ANF and LAP was steeper with ET-1 than with saline or verapamil (both P less than 0.05), indicating that the enhanced ANF secretion with ET-1 was occurring at all levels of LAP. Thus volume-induced secretion of ANF is not suppressed by verapamil, but is directly enhanced by low-dose ET-1, known to activate the phosphoinositide pathway.

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