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Abstract

As the world faces an obesity “epidemic,” there is a need to better understand the mechanisms by which overweight is translated into insulin resistance, hypertension, and diabetes. Although the processes of transition remain uncertain, overactivity of the sympathetic nervous system appears to be pivotal. In human obesity, there is stimulation of the sympathetic outflow to the kidneys, evident in increased rates of spillover norepinephrine into the renal veins, and to the skeletal muscle vasculature, demonstrated with microneurography. The cause is unclear, but may involve the stimulatory action of leptin released from adipose tissue, or from within the brain, for which there is recent evidence in human obesity. The high renal sympathetic tone contributes to the development of hypertension in the obese, by stimulating renin secretion and through promoting renal tubular reabsorption of sodium. Neurally mediated skeletal muscle vasoconstriction reduces glucose delivery and uptake in muscle. Impairment of glucose uptake by skeletal muscle is a hallmark of insulin resistance syndromes.

Pharmacological modulation of the sympathetic nervous system, with imidazoline receptor binding agents such as rilmenidine is a promising therapeutic approach for favourably modifying insulin sensitivity in obesity and obesity-related hypertension. This finding has relevance to the potential use of imidazoline receptor agents in the treatment of hypertensive diabetic patients. In the hypertension accompanying maturity-onset obesity, with recent recommendations from advisory bodies setting lower goal for blood pressures, and with these lower targets often being reached only with combinations of antihypertensive agents, it is advisable that all drugs used in combination therapy have a favourable, or at least neutral effect on insulin resistance.

Hypertension, norepinephrine, insulin resistance, imidazoline receptor, obesity, diabetes
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© American Journal of Hypertension, Ltd. 2001
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