Key result
High fat diet feeding in rats significantly increased the maximal in vitro contractile responses of the thoracic aorta to 5-Hydroxytryptamine and Angiotensin II compared to a normal diet.
Why the study?
Does a high fat diet increase vascular contractile responses to 5-hydroxytryptamine and Angiotensin II in male Sprague Dawley rats?
Does a high fat diet increase vascular contractile responses to 5-hydroxytryptamine and Angiotensin II in male Sprague Dawley rats?
Answers are grounded in this paper and cite their sources.
A high fat diet in rats increases maximal in vitro vascular contractile responses to 5-hydroxytryptamine and Angiotensin II, potentially contributing to hypertension in metabolic syndrome.
BACKGROUND: Feeding normal rats with high dietary levels of saturated fat leads to pathological conditions, which are quite similar to syndrome X in humans. These conditions such as hypertriglyceridemia, hypercholesterolemia, obesity, and hyperglycemia might induce hypertension through various mechanisms. Metabolic syndrome and the resulting NIDDM represent a major clinical challenge because implementation of treatment strategies is difficult. Vascular abnormalities probably contribute to the etiology of many diabetic complications including nephropathy, neuropathy, retinopathy, and cardiomyopathy. It has been shown that in Streptozotocin induced diabetic animals there is an increase in maximal responses to 5-Hydroxytryptamine and Angiotensin II. The purpose of this study was to evaluate High fat diet fed rats for the development of hypertriglyceridemia, hypercholesterolemia, hyperinsulinemia and hyperglycemia and to assess their vascular responses to 5-Hydroxytryptamine and Angiotensin II. METHODS: Male Sprague Dawley rats were used for this study and were divided into two equal groups. One of the groups was fed with normal pellet diet and they served as the control group, whereas the other group was on a high fat diet for 4 weeks. Body weight, plasma triglycerides, plasma cholesterol, and plasma glucose were measured every week. Intraperitoneal glucose tolerance test was performed after 4 weeks of feeding. At the end of fourth week of high fat diet feeding, thoracic aortae were removed, and cut into helical strips for vascular reactivity studies. Dose-response curves of 5-Hydroxytryptamine and Angiotensin II were obtained. RESULTS: There was no significant difference in pD2, with 5-Hydroxytryptamine and Angiotensin II in both groups but Emax was increased. CONCLUSIONS: These results suggest that hypertension in high fat diet rats is associated with increased in vitro vascular reactivity to 5-HT and Ang II.
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Ghatta et al. (2004) studied Metabolic syndrome / Insulin resistance. High fat diet vs. Normal pellet diet was evaluated on Maximal contractile response (Emax) to 5-Hydroxytryptamine (5-HT) (p=<0.01). High fat diet feeding in rats significantly increased the maximal in vitro contractile responses of the thoracic aorta to 5-Hydroxytryptamine and Angiotensin II compared to a normal diet.
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