PS 11-76 UPREGULATION OF MLCK AND ACTIVATION OF CPI-17 ARE RESPONSIBLE FOR HIGH FAT DIET –INDUCED VASCULAR HYPER-CONTRACTILITY AND HYPERTENSION

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Abstract

Objective:

Recently, obese population is growing really fast world-wide. It is well demonstrated that obesity is risk factor for the hypertension. Although renin-Angiotensin-Aldosterone system component is increased in obese people and blocking angiotensin II type1 (AT1) receptor greatly reduced blood pressure, direct evidence that explains the underlying mechanism for increased vascular contractility is missing. Here, we tested hypothesis that the regulatory proteins which modulate the myosin phosphorylation were altered with high fat diet.

Design and Method:

8 week male Sprague-Dawley rats were fed with 60% cholesterol diet or normal diet for 4 months. Body weight, plasma lipid profile, blood pressure (BP), angiotensin II (Ang II)-induced aortic constriction, and expression of vascular contraction regulating proteins were determined.

Results:

As a result, high fat diet increased body weight. BP and Ang II-induced aortic contraction were also increased. Expression of p-CPI-17 and myosin light chain (MLC) kinase was increased by high fat diet along with increased phosphorylation of MLC.

Conclusions:

In conclusion obesity-induced hypertension is through increased vascular contractility via increased expression and activation of contractile proteins and subsequent MLC phosphorylation.

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