Effect of moderately high dietary salt and lipoic acid on blood pressure in Wistar-Kyoto rats.

Background: Approximately one-half of hypertensive individuals are salt sensitive, and animal models of human hypertension also exhibit increased blood pressure when exposed to high-salt diets. Salt sensitivity is associated with insulin resistance, which results in altered glucose metabolism, increasing aldehydes. Previously, the authors have shown that a high-salt diet (8% NaCl) caused an increase in blood pressure, tissue aldehyde conjugates and cytosolic free calcium, with resulting adverse renal vascular changes, in Wistar-Kyoto rats.

Fructose-induced hypertension in Wistar-Kyoto rats: interaction with moderately high dietary salt.

We investigated the effects of 4% fructose plus moderately high salt (MHS) (4% NaCl) treatment on tissue aldehyde conjugates, platelet cytosolic free calcium ([Ca2+]i), renal morphology, and systolic blood pressure (SBP) in Wistar-Kyoto rats, and whether these effects were reversible (R) after withdrawal of treatment. At age 7 weeks, rats were divided into 4 groups: NS group, given normal salt (NS) diet (0.7% NaCl) for 18 weeks; NS+F(R) group, NS diet and fructose in water for 14 weeks, then 4 weeks fructose withdrawal; MHS+F group, NS diet and fructose for 6 weeks, then MHS diet and fructose for 12 weeks; and MHS+F(R) group, NS diet and fructose for 6 weeks, then MHS diet and fructose for 8 weeks, then MHS and fructose withdrawal for 4 weeks.

Low ethanol intake prevents salt-induced hypertension in WKY rats.

Low alcohol intake in humans lowers the risk of coronary heart disease and may lower blood pressure. In hypertension, insulin resistance with altered glucose metabolism leads to increased formation of aldehydes. We have shown that chronic low alcohol intake decreased systolic blood pressure (SBP) and tissue aldehyde conjugates in spontaneously hypertensive rats and demonstrated a strong link between elevated tissue aldehyde conjugates and hypertension in salt-induced hypertensive Wistar-Kyoto (WKY) rats.

Dietary lipoic acid supplementation attenuates hypertension in Dahl salt sensitive rats.

There is strong evidence that excess dietary salt (NaCl) is a major factor contributing to the development of hypertension. Salt sensitive humans and rats develop hypertension even on a normal salt diet. Salt sensitivity is associated with glucose intolerance and insulin resistance in both humans and animal models, including Dahl salt sensitive (DSS) rats.

Dietary vitamin e supplementation attenuates hypertension in Dahl salt-sensitive rats.

There is strong evidence that excess dietary salt (NaCl) is a major factor contributing to the development of hypertension. Salt-sensitive humans and rats develop hypertension even on a normal-salt diet. Salt sensitivity is associated with glucose intolerance and insulin resistance in both humans and animal models, including Dahl salt-sensitive (DSS) rats.