Abstract

Lipoprotein lipase (LPL) is an endothelium-bound enzyme that is rate determining for the clearance of triacylglycerol-rich lipoproteins. We assessed cardiac heparin-releasable LPL activity in an acquired model of hypertension, the fructose-hypertensive rat. Fructose feeding (10% solution in drinking water ad libitum) for 2 (short-term) or 4-6 (long-term) weeks induced hypertension, hypertriglyceridemia, and hyperinsulinemia in male Wistar rats. After short- and long-term fructose treatment, LPL activity in coronary perfusates was determined by retrogradely perfusing the hearts with heparin. Short-term fructose treatment did not alter cardiac heparin-releasable LPL activity, whereas a significant decrease in LPL activity was seen in the long-term treated group. Discontinuation of fructose treatment for 2 weeks from the long-term group normalized blood pressure and cardiac heparin-releasable LPL activity. Interestingly, acute vasodilation by in vitro perfusion of coronary vasodilators like nifedipine and CGS-21680 increased cardiac heparin-releasable LPL activity in the long-term group to control levels. These studies demonstrate that long-term fructose-induced hypertension may play a significant role in regulating cardiac LPL activity. Whether or not this altered LPL activity has a role in the regulation of fatty acid supply to the hypertensive heart has yet to be determined.

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