Plasma atrial natriuretic factor during chronic thoracic inferior vena caval constriction.
The effects of chronic constriction of the thoracic inferior vena cava (TIVCC) on plasma atrial natriuretic factor (pANF) were studied in conscious dogs (n = 5). TIVCC decreased left and right atrial pressure and led to a decrease in pANF concentration from 199 +/- 12 to 104 +/- 14 pg/ml while plasma renin and vasopressin concentrations increased. These hormonal changes were associated with a significant fall in sodium excretion to less than 5 meg/day. pANF remained suppressed during chronic TIVCC as the dogs expanded their extracellular fluid volume and developed ascites. Acute release of TIVCC resulted in abrupt increases in left and right atrial pressure but only a modest rise in pANF from 96 +/- 16 to 185 +/- 45 pg/ml. The magnitude of the rise in pANF (twofold) contrasted sharply with the eightfold increase in sodium excretion that occurred over the first 24 hours. Our data suggest that decrease in atrial pressure below normal results in a decline in pANF, which, acting in concert with the activated renin-angiotensin system and vasopressin, may contribute to sodium retention. On the other hand, during acute release of TIVCC, which markedly increased atrial pressure and sodium excretion, pANF only returned to control levels. These data suggest that ANF release may be attenuated during chronic reduction in atrial pressure and also raise a question concerning the magnitude of the primary role of ANF in this natriuretic response.
D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood; D009320:Atrial Natriuretic Factor / Q000097:blood*; D001794:Blood Pressure; D004285:Dogs; D008297:Male; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism; D014661:Vasoconstriction; D014682:Vena Cava, Inferior / Q000502:physiology*
D001127:Arginine Vasopressin; D009320:Atrial Natriuretic Factor; D012964:Sodium; D012083:Renin