Potential Mechanisms Responsible for Deficient Skin Vasodilatation to Mental Stress in Obesity

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Several mechanisms could possibly lead to the observed impairment in skin vasodilatation to mental stress in obesity. Skin vasodilatation in response to mental stress in humans occurs due to both local sympathetic nerve traffic withdrawal and b2-adrenergic vasodilatation from circulating epinephrine and norepinephrine. It is possible that circulating norepinephrine causes vasodilatation by stimulating b-adrenoreceptors located predominantly on the inner layer of smooth muscle. Given that nerve terminals are located in the adventitia of the blood vessels, neurally released norepinephrine causes vasoconstriction by stimulation of a-adrenoreceptors, located predominantly in the outer layer of vascular smooth muscle [14]. The sympathetic withdrawal during mental stress might be attenuated, because it is known that baroreflex control of muscle sympathetic nerve activity is impaired in obesity and improves with weight loss in obese individuals. There is an endothelium-dependent component of b2-adrenergic vasodilatation in the human forearm microvasculature. There is also a choliner-gic system in human endothelium. Endothelium-dependent forearm vasodilatation to mental stress is associated with cholinergic stimulation of the vascular endothelium. Obesity without complications leads to endothelial dysfunction in forearm resistance vessels, and skin microvasculature constitutes a significant component of the forearm vascular bed. Forearm vasodilatation to mental stress is endothelium dependent. Obesity is associated with defective b2-adrenergic vasodilatation in the human forearm. Obesity-associated endothelial dysfunction may lead to deficient skin vasodilatory response to mental stress and, therefore, may account for the development of hypertension and cardiovascular disease in obese individuals.

In addition, insulin resistance might play a role in abnormal microcirculatory responses to mental stress in obesity. It is known that obesity leads to insulin resistance. Many obese individuals have insulin resistance but normal fasting glucose values. Skin capillary recruitment and acetyl-choline-mediated vasodilatation have a strong and positive correlation with insulin sensitivity. A reduction in skin microvascular vasodilator response to ischemia and acetylcholine is associated with insulin resistance [9]. Deficiency of skin microvascular dilatation has also been associated with higher 24-hour systolic blood pressures [9]. Exaggerated blood pressure increase to mental and physical stress has been observed in normotensive obese women with insulin resistance and abnormal glucose tolerance tests. Endothelial dysfunction appears to contribute to the absence of insulin-induced vasodilatation in obesity [15].

Adipose tissue has a local renin-angiotensin system. Angiotensinogen, angiotensin-converting enzyme, and AT1 and AT2 receptors are all present in human adipose tissue. Angiotensinogen expression in adipose tissue correlates with waist-to-hip ratio in obese humans. Central fat distribution is associated with increased systemic vascular resistance and hypertension. Increased activity of this local renin-angiotensin system may impair skin vasodilatation in obesity. Also, increased levels of proinflammatory cytokines might play a role, because chronic subclinical inflammation was shown to be a part of the insulin resistance syndrome. C-reactive protein has been shown to positively correlate with measures of obesity, such as body mass index and waist circumference. Tumor necrosis factor-a and interleukin-6 concentrations are higher in obese individuals. Weight loss leads to a decrease in the levels of these proinflammatory cytokines, along with a decrease in adhesion molecules and improvement in endothelial function.

Elevated free fatty acid secretion by adipose tissue in obesity may adversely affect skin microvascular function, because these lipid metabolites have been shown to impair endothelium-dependent vasodilatation at the microcircula-tory level [15] and to increase vasoconstrictor responses in dorsal hand veins [16].

Obese individuals are known to have increased levels of low-density lipoprotein (LDL) cholesterol and triglycerides and decreased high-density lipoprotein (HDL) cholesterol. In healthy women, skin vasodilatation in response to iontophoresis of acetylcholine, isoprenaline, and nitroprus-side has been shown to be positively correlated to HDL cholesterol, and negatively correlated to the ratio of total cholesterol/HDL and triglycerides [4]. Skin postischemic microcirculatory dilatation is blunted in patients with hypertriglyceridemia [17].

Further studies are necessary to evaluate the significance of all the potential mechanisms just described in relation to skin microcirculatory impairments in obesity.

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