Ventricles as a major site of atrial natriuretic factor synthesis and release in cardiomyopathic hamsters with heart failure.

A quantitative in vitro autoradiographic study was performed on the aorta, renal glomeruli, and adrenal cortex of cardiomyopathic hamsters in various stages of heart failure and correlated, in some instances, with in vivo autoradiography. The results indicate virtually no correlation between the degree of congestive heart failure and the density of 125I-labeled atrial natriuretic factor [(Ser99, Tyr126)ANF] binding sites (Bmax) in the tissues examined. Whereas the Bmax was increased in the thoracic aorta in moderate and severe heart failure, there were no significant changes in the zona glomerulosa. The renal glomeruli Bmax was lower in mild and moderate heart failure compared with control and severe heart failure. The proportion of ANF B- and C-receptors was also evaluated in sections of the aorta, adrenal, and kidney of control and cardiomyopathic hamsters with severe heart failure. (Arg102, Cys121)ANF [des-(Gln113, Ser114, Gly115, Leu116, Gly117) NH2] (C-ANF) at 10(-6) M displaced approximately 505 of (Ser99, Tyr126)125I-ANF bound in the aorta and renal glomeruli and approximately 20% in the adrenal zona glomerulosa in both series of animals. These results suggest that ANF may exert a buffering effect on the vasoconstriction of heart failure and to a certain extent may inhibit aldosterone secretion. The impairment of renal sodium excretion does not appear to be related to glomerular ANF binding sites at any stage of the disease.

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Catecholamine, dopamine-ß-hydroxylase and atrial natriuretic factor content in separate heart chambers of cardiomyopathic hamsters

Life Sciences ◽

10.1016/0024-3205(87)90547-9 ◽

1987 ◽

Vol 41 (20) ◽

pp. 2333-2338 ◽

Cited By ~ 4

Author(s):

Otto Kuchel ◽

Marc Cantin ◽

Nguyen T. Buu ◽

Waldemar Debinski ◽

Gaétan Jasmin ◽

...

Keyword(s):

Atrial Natriuretic Factor ◽

Factor Content ◽

Natriuretic Factor ◽

Cardiomyopathic Hamsters ◽

Atrial Natriuretic

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.4.h1441 ◽

1996 ◽

Vol 271 (4) ◽

pp. H1441-H1448 ◽

Cited By ~ 18

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.

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Effects of dobutamine and salbutamol on haemodynamics and atrial natriuretic factor in patients with severe congestive heart failure

Clinical Physiology ◽

10.1111/j.1475-097x.1991.tb00451.x ◽

1991 ◽

Vol 11 (3) ◽

pp. 199-210 ◽

Cited By ~ 2

Author(s):

N. Keller ◽

R. Sykulski ◽

J. Larsen

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Atrial Natriuretic Factor ◽

Severe Congestive Heart Failure ◽

Natriuretic Factor ◽

Atrial Natriuretic

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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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