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      High-fat diet elevates blood pressure and cerebrovascular muscle Ca(2+) current.


      Animals, Blood Pressure, drug effects, Calcium, metabolism, Calcium Channels, physiology, Cerebrovascular Circulation, Cholesterol, analysis, blood, Chromatography, High Pressure Liquid, Dietary Fats, pharmacology, Disease Models, Animal, Fatty Acids, Nonesterified, Hyperlipidemias, physiopathology, Hypertension, Ion Channel Gating, Kinetics, Male, Muscle, Smooth, Vascular, chemistry, Obesity, Patch-Clamp Techniques, Rats, Rats, Inbred Strains

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          Dietary fat contributes to the elevation of blood pressure and increases the risk of stroke and coronary artery disease. Previous observations have shown that voltage-gated Ca(2+) current density is significantly increased in hypertension and can be affected by free fatty acids (FAs). We hypothesized that a diet of elevated fat level would lead to an increase in blood pressure, an elevation of L-type Ca(2+) current, and an increase in saturated FA content in vascular smooth muscle cell membranes. Male Osborne-Mendel rats were fed normal rat chow or a high-fat diet (Ob/HT group) for 8 weeks. Blood pressures in the Ob/HT group increased moderately from 122.5+/-0.7 to 134.4+/-0.8 mm Hg (P<0.05, n=26). Voltage-clamp examination of cerebral arterial cells revealed significantly elevated L-type Ca(2+) current density in the Ob/HT group. Voltage-dependent inactivation of the Ob/HT L-type channels was significantly delayed. Total serum FA contents were significantly elevated in the Ob/HT group, and HPLC analyses of fractional pools of FAs from segments of abdominal aorta revealed that arachidonic acid levels were elevated in the phospholipid fraction in Ob/HT. No differences in vascular membrane cholesterol contents were noted. Plasma cholesterol was significantly elevated in portal venous and cardiac blood samples from Ob/HT rats. These findings suggest that an elevation of plasma FAs may contribute to the development of hypertension via a process involving the elevation of Ca(2+) current density and an alteration of channel kinetics in the vascular smooth muscle membrane.

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