Hypotensive hemorrhage (HH) is characterized by intravascular volume depletion, avid renal sodium retention, and activation of the renin-angiotensin-aldosterone system (RAAS). The current studies were designed to investigate whether intravascular volume depletion would modulate circulating atrial natriuretic factor (ANF) and, further, to examine that contribution, if any, a decrease in ANF would have in mediating the antinatriuresis and RAAS stimulation associated with HH. Two groups of anesthetized dogs underwent controlled arterial hemorrhage to reduce mean arterial pressure by 15-20 mmHg. Data were collected before and immediately after HH. One group (n = 6) underwent hemorrhage alone, whereas a second group (n = 5) underwent HH with simultaneous administration of α-human ANF (2.5 ng·kg-1·min-1), a dose calculated to prevent a reduction in ANF. In the untreated group, circulating ANF was significantly reduced after hemorrhage (79.4 ± 7.4 to 57.2 ± 3.4 pg/ml, P < 0.05), whereas in the treated group ANF increased significantly (73.5 ± 12.2 to 147.4 ± 17.2 pg/ml, P < 0.05). Despite differences in circulating ANF, both groups had similar reductions in urinary sodium excretion and renal blood flow, and similar increases in plasma renin activity. These studies demonstrate that circulating ANF is significantly reduced in HH; however, the mechanisms of antinatriuresis and activation of the RAAS is independent of the reduction in circulating ANF.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - Jan 1 1988|
ASJC Scopus subject areas
- Physiology (medical)