Role of angiotensin II in high fructose-induced left ventricular hypertrophy in rats.

Abstract

Recent studies suggest the linkage of hypertension and insulin resistance. High fructose diet is known to induce hyperinsulinemia and hypertension in rats. In a previous study, however, high fructose (66%) diet failed to elevate blood pressure but increased left ventricular weight in Sprague-Dawley rats. In the present study, we investigated the precise mechanism of high fructose diet-induced changes in the cardiovascular system in rats. Intake of fructose-enriched diet for 2 weeks increased serum insulin and plasma angiotensin II levels. Urinary excretion of sodium and norepinephrine was not changed. Blood pressure measured directly through an indwelling catheter was not increased, but left ventricular weight and protein content were increased by high fructose diet To further elucidate the role of the renin-angiotensin system, an angiotensin II type 1 receptor antagonist, TCV-116, was given orally at 1 nig/kg per day with either normal or high fructose diet Concomitant administration of TCV-116 did not affect plasma glucose or serum insulin levels. Plasma angiotensin II was increased, but neither urinary sodium nor norepinephrine was changed by TCV-116. 3 Inhibition of insulin secretion by a somatostatin analogue 4 or reduction of insulin resistance by exercise 5 prevents hypertension, suggesting an etiological role of hyperinsulinemia in the elevation of blood pressure. In a preliminary study, 6 we showed that high fructose diet failed to increase blood pressure but induced left ventricular (LV) hypertrophy in rats. Serum insulin and plasma angiotensin II (Ang II) were increased by high fructose diet, suggesting a possible role of either insulin or Ang II in LV hypertrophy. However, the precise mechanism is not clear.The present study examined the mechanism of the development of LV hypertrophy induced by high fructose diet. Insulin causes sodium retention by increasing proximal tubular reabsorption 7 and activating the sym-

The Vascular Renin-Angiotensin System as a Possible Source of Vascular Inflammation in Fructose-Fed Rats

“…From this point of view, it is noteworthy that the treatment with captopril did not alleviate hyperinsulinemia or glucose intolerance, which is in keeping with a previous study (7). Although insulin sensitivity was not directly measured by more sophisticated techniques such as glucose clamp, these findings have several implications.…”

Insulin-Mediated Growth in Aortic Smooth Muscle and the Vascular Renin-Angiotensin System

“…Most reports describing a relationship between insulin and the RAS have been in whole animal models 37 describing systemic effects. Thus, Kobayashi et al 38 and Iyer et al 39 reported elevated levels of plasma Ang II in the insulin-resistant, hyperinsulinemic, fructose-fed rat model. These studies did not resolve whether the high insulin levels were the cause of the elevated plasma Ang II.…”

A high-fructose diet induces insulin resistance but not blood pressure changes in normotensive rats

“…Furthermore, circulating catecholamines are elevated in sucrose-fed rats on a high-salt diet, and it has been proposed that these mediators may contribute to hypertension through their vasoconstrictive and/or antinatriuretic properties (28)(29)(30). However, catecholamines are probably not the only vasoconstrictive factors involved in the development of hypertension in fructose-fed rats.…”