Endogenous atrial natriuretic factor in dogs with caval constriction.
Chronic constriction of the thoracic inferior vena cava results in decreased filling pressure and cardiac output, in augmented secretion rates of renin and aldosterone, and in marked sodium retention with ascites and edema formation. The goal of the present study was to determine temporal changes in the plasma concentration of immunoreactive atrial natriuretic factor (iANF) in response to chronic constriction of the thoracic inferior vena cava in the conscious dog. Following constriction of the thoracic inferior vena cava, all dogs retained sodium avidly for at least 10 days, and both plasma renin activity and plasma aldosterone concentration increased markedly (p less than 0.05). Additionally, the baseline plasma iANF of 70 +/- 5 pg/ml decreased significantly to 24 +/- 7, 26 +/- 10, and 34 +/- 11 pg/ml (p less than 0.05) on days 2, 6, and 10 following thoracic inferior vena cava constriction. Thus, chronic sodium retention in this model is associated with prolonged endocrine adjustments in the circulating levels of renin-aldosterone and iANF. We suggest that chronic decreases in the secretion of atrial natriuretic factor might contribute to the inability of the dog with constriction of the thoracic inferior vena cava to excrete sodium normally.
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood*; D002496:Central Venous Pressure; D003251:Constriction, Pathologic / Q000097:blood; D004285:Dogs; D005260:Female; D009318:Natriuresis; D009994:Osmolar Concentration; D014652:Vascular Diseases / Q000097:blood / Q000503:physiopathology / Q000652:urine; D014682:Vena Cava, Inferior
D009320:Atrial Natriuretic Factor