Insulin resistance, increased leptin and free fatty acids levels are thought to be factors that increase sympathetic nervous activation in those with metabolic syndrome. Elevated resting heat rates and baroreflex dysfunction have been reported to play an important role in development of hypertension in metabolic syndrome. Scientific studies indicate that free fatty acids raise blood pressure, heart rate, and α 1-adrenoceptor vasoreactivity, while reducing baroreflex sensitivity, endothelium-dependent vasodilatation, and vascular compliance.
Leptin is a hormone produced by adipocytes (fat cells).Insulin resistance increases leptin levels. Increased leptin levels have been reported to elevate sympathetic nervous system activity suggesting that leptin-dependent sympathetic nervous activation may contribute to obesity associated hypertension.
Catecholamines such as epinephrine & norepinephrine act as hormones or neurotransmitters. They have a powerful effect on blood pressure. Catecholamine concentrations and muscle sympathetic nervous activity are increased in obese individuals as compared with lean individuals. Additionally, muscle sympathetic nervous activity in individuals with central obesity (belly fat) is significantly greater than those in individuals with peripheral obesity (overall body weight).
Keep in mind, for those with excess weight and/or excess belly fat, weight loss can lessen the catecholamine and sympathetic blood vessel tightening (vasoconstriction) mechanisms that can contribute to hypertension.
Sources: Non-esterified fatty acids and blood pressure elevation: a mechanism for hypertension insubjects with obesity/insulin resistance? The underlying mechanisms for the development of hypertension in the metabolic syndrome.
Insulin resistance and the sympathetic nervous system.
Egan BM
Curr Hypertens Rep 2003, 5:247-254
Sarafidis PA, Bakris GL
J Hum Hypertens 2007, 21:12-9.
Hidekatsu Yana, Yoshiharu Tomona
Nutrition Journal 2008

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Posted by: Acai Optimum | May 17, 2010 at 04:57 AM