Action of endogenous atrial natriuretic peptide in calves with experimental acute central venous congestion and low cardiac output.
OBJECTIVE
The aim of the study was to investigate plasma concentrations of atrial natriuretic peptide, aldosterone, and renin during experimentally induced acute central venous congestion.


METHODS
Two experimental calf models were used: (1) right heart failure due to pulmonary artery obstruction; (2) inferior vena cava syndrome produced by inferior vena caval obstruction. Hormonal responses and haemodynamic variables were measured over 6 h.


METHODS
Experiments were performed on three female "Schwarzbund" calves, age 3 months, weight 92 +/- 8 kg.


RESULTS
In the pulmonary artery obstructed group there was an increase of plasma aldosterone from 6.5(SEM 1.6) to 22.1(3.2) ng.dl-1 (p less than 0.05), of renin from 0.7(0.1) to 2.5(0.3) Goldblatt units x 10(-4).ml-1 (p less than 0.05), and of atrial natriuretic peptide from 22.1(4.5) to 141.4(27.8) pmol.litre-1 (p less than 0.05). During inferior vena caval obstruction, aldosterone increased from 2.4(0.4) to 20.9(2.0) ng.dl-1 (p less than 0.05), and renin increased from 0.4(0.05) to 2.0(0.20) Goldblatt units x 10(-4).ml-1 (p less than 0.05). In this experiment, atrial natriuretic peptide remained unchanged. Cardiac output decreased in both groups. There was significant fluid and electrolyte retention during both experiments, with urine volume decreasing from 87.7(11.6) to 35.0(1.2) ml-h-1 in experiment (1), and from 185(14) to 95.7(8.6) ml.h-1 in experiment (2).


CONCLUSIONS
The study suggests (1) that in an experimental acute state of reduced cardiac output due to pulmonary artery stenosis with constantly increased right heart pressures, raised endogenous atrial natriuretic peptide failed to induce diuresis and natriuresis; (2) that in acute right heart failure, renin and aldosterone secretion could not be suppressed by raised atrial natriuretic peptide concentrations; and (3) atrial natriuretic peptide secretion seemed to be exhausted after 6 h continuous atrial distension.
Rokitansky
A M
AM
Second Department of Surgery, University of Vienna, General Hospital, Austria.
Losert
U M
UM
Trubel
W
W
Wieselthaler
G
G
Krausler
S
S
Shreiner
W
W
Buxbaum
P
P
Vierhapper
H
H
Waldhäusl
W K
WK
Wolner
E
E
D000208:Acute Disease; D000450:Aldosterone / Q000097:blood; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood* / Q000502:physiology; D001794:Blood Pressure; D002302:Cardiac Output / Q000502:physiology; D002303:Cardiac Output, Low / Q000097:blood* / Q000150:complications / Q000503:physiopathology / Q000652:urine; D002417:Cattle; D002496:Central Venous Pressure; D003251:Constriction, Pathologic; D004231:Diuresis / Q000502:physiology; D004573:Electrolytes / Q000652:urine; D005260:Female; D006325:Heart Atria / Q000503:physiopathology; D011651:Pulmonary Artery / Q000503:physiopathology; D012083:Renin / Q000097:blood; D013577:Syndrome; D014682:Vena Cava, Inferior / Q000503:physiopathology*
D004573:Electrolytes; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012083:Renin