Impact of fructose feeding on the control of cardiac oxygen consumption by NO‐superoxide interaction during pregnancy

Abstract

Fructose consumption (FC) has caused much concern because of its prominence in today's diet and its implication in cardiovascular disease. We hypothesized that FC alters cardiac metabolism by generating superoxide, which reduces NO bioavailability. We then extended the study to the heart during pregnancy where NO plays an essential role in its successful completion. Female SD rats (N=16) were fed either a normal or a 60% purified fructose diet for 21 days. Hemodynamic and metabolic measurements showed significant increases in diastolic and mean arterial pressures, and insulin levels (3.10 ± 0.42 to 5.47 ± 0.44 ng/mL) with FC. The ability of bradykinin to reduce myocardial O2 consumption (MVO2) in vitro was impaired by FC (28.46 ± 2.30% to 16.59 ± 1.64%). This effect was reversed by apocynin or tiron, which inhibits NADPH oxidase and scavenge superoxide, respectively. MVO2 decrease by bradykinin with L‐NAME, an eNOS inhibitor, was comparable to that in rats with FC. In pregnant SD rats (N=16), a reduction in the ability of NO to control MVO2 with FC was also exhibited, along with significant increases in diastolic, systolic and mean arterial pressures. We conclude that a high‐fructose diet lowers NO bioavailability through the generation of superoxide, alters the control of arterial pressures, and disrupts the regulation of O2 consumption in the normal myocardium, especially during pregnancy. Supported by HL43023, 50142