Determinants of coronary effects of atrial natriuretic factor in dogs
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Abstract. The direct vascular action of atrial natriuretic factor (ANF) is unclear. In coronary vasculature, vasodilation has been reported as well as vasoconstric‐tion. Doses of ANF, baseline plasma ANF levels and interference with the renin‐angiotensin system might account for the controversy. We tried to further analyse determinants of the effect of ANF on coronary blood flow in anaesthetized dogs. The chest was opened and the left anterior descending coronary artery cannulated and perfused at constant normal (= 76 ±5 mmHg, n= 10) or reduced (= 37 ± 3 mmHg, n= 10) pressure from the femoral arteries. At normal coronary perfusion pressure, ANF (1 ng kg‐1 i.c.) reduced coronary flow from 30.7 ± 4.2 to 26.9 ± 4.0 ml min‐1 (P<0.05). This effect was no longer significant at reduced coronary perfusion pressure (4.9 ± 0.8 vs. 4.6 ± 0.7 ml min‐1). ANF (1 ng kg‐1 i.c.) reduced coronary blood flow in correlation with baseline plasma ANF levels (r= 0.77, P< 0.001). However the large variability of the constrictor effect of ANF in the rather small range of baseline plasma ANF, weakens the importance of this result and suggests other additional determinants. ANF (100 ng kg‐1 i.e.) significantly increased coronary blood flow by 16–23% (P<0.05). In a second series of experiments, the converting enzyme inhibitor captopril (0.25 mg kg‐1 i.c. followed by 0.25 mg kg‐1 h‐1, i.c., n= 8) and the angiotensin II receptor blocker saralasin (1 μg kg‐1 min‐1, i.c., n=9) significantly reduced the coronary dilator effect of ANF while coronary flow was similar after repeated injections in control animals (n= 6). Thus, lower doses (1 ng kg‐1 i.c.) of ANF may induce coronary constriction. The occurrence and extent of coronary constriction is variable and depends to some extent on baseline ANF levels. Higher doses of ANF (100 ng kg‐1 i.c.) consistently induce coronary dilatation which results at least in part from interference with the renin‐angiotensin system.
