Increased ANF secretion after volume expansion is preserved in rats with heart failure
Chien, Y.W.; Barbee, R.W.; MacPhee, A.A.; Frohlich, E.D.; Trippodo, N.C.
American Journal of Physiology 254(2 Pt 2): R185-R191
1988
ISSN/ISBN: 0002-9513 PMID: 2964205 Document Number: 324951
To examine whether the failing heart has reached a maximal capacity to increase plasma atrial natriuretic factor (ANF) concentration, the change in plasma immunoreactive ANF level due to acute blood volume expansion was determined in conscious rats with chronic heart failure. Varying degrees of myocardial infarction and thus heart failure were induced by coronary artery ligation 3 wk before study. Compared with controls, infarcted rats had decreases in mean arterial pressure (-10 mmHg, P < 0.01), cardiac index (-27%, P < 0.001), renal blood flow (-35%, P < 0.01), and peak left ventricle-developed pressure after aortic occlusion (an index of pressure generating ability; -15%, P < 0.01), and increases in central venous pressure (+ 1.7 mmHg, P < 0.01), left ventricular end-diastolic pressure (+ 10 mmHg, P < 0.001), total peripheral resistance (+ 28%, P < 0.01), and plasma ANF level (752 .+-. 109 vs. 244 .+-. 33 pg/ml, P < 0.001). Plasma ANF was correlated with infarct size, cardiac filling pressures, and left ventricule pressure-generating ability. At 5 min after 25% blood volume expansion, plasma ANF in rats with heart failure increased by 2,281 .+-. 345 pg/ml; the magnitude of the changes in circulating ANF and hemodynamic measurements was similar in controls. The results suggest that plasma ANF level can be used as a reliable index of the severity of heart failure, and that the capacity to increase plasma ANF concentration after acute volume expansion is preserved in rats with heart failure. There was no evidence of a relative deficiency of circulating ANF in this model of heart failure.